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ABSTRACT |
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INTRODUCTION
METHODS
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DISCUSSION
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Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality. Free oxygen radicals have been implicated in the pathogenesis of cardiovascular disorders. Therefore, we aimed to test the hypothesis that increased oxidative stress constitutes one underlying mechanism for the connection between OSA and cardiovascular disease. In 18 patients with OSA the release of superoxide from polymorphonuclear neutrophils was determined after stimulation with the bacterial tripeptide formylmethionylleucylphenylalanine (fMLP) and the calcium ionophore A23. Superoxide production was measured as superoxide dismutase-inhibitable reduction of cytochrome c. Blood samples were obtained before and after two nights of CPAP therapy and after 4.8 ± 0.6 mo of follow-up. Ten healthy young volunteers and 10 lung cancer patients without OSA but a similar spectrum of comorbidity served as controls. Before CPAP, neutrophil superoxide generation was markedly enhanced in OSA when compared with both control groups. Effective CPAP therapy led to a rapid and long-lasting decrease of superoxide release in OSA. In conclusion, OSA is linked with a "priming" of neutrophils for enhanced respiratory burst. The increased superoxide generation, which might have major impact on the development of cardiovascular disorders, is virtually fully reversed by effective CPAP therapy.
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INTRODUCTION |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Obstructive sleep apnea (OSA) is associated with cardiovascular morbidity such as arterial hypertension, coronary artery disease, and cerebrovascular disease (1). It is thought that these disorders account for the increased mortality observed in OSA (2); however, the causal relationship between OSA and cardiovascular disease remains to be clearly established (3).
Free oxygen radicals are highly reactive molecules playing pivotal roles in the pathophysiology of such different diseases as neurodegenerative disorders, chronic inflammatory disease, and cancer (4). Free oxygen radicals are also supposed to make important contributions to the development of cardiovascular disease (5, 6). This has, for example, been shown for the process of ischemia/reperfusion injury in coronary artery disease. Under these conditions, polymorphonuclear neutrophils are activated, with decreasing tensions of oxygen being considered as one of the triggers, to adhere to the endothelium and to release free oxygen radicals. The enhanced free radical generation contributes to postischemic cellular injury and extension of infarct size (7).
In OSA repeated collapse of the upper airways occurs during sleep. Consequently, cyclical alterations of arterial oxygen saturation are observed, with oxygen desaturation developing in response to apneas followed by resumption of oxygen saturation during hyperventilation. This phenomenon has been referred to as hypoxia/reoxygenation and may to some extent be compared with the sequelae in ischemia/reperfusion, although overall changes being by far not so drastic. However, even minor abnormalities related to the hypoxia/reoxygenation events may be of interest against the background that these events may occur frequently and over long time periods in untreated patients with OSA.
On the basis of these considerations, it was hypothesized that OSA may be linked with increased oxidative stress (10). This issue has already been addressed in a previous study by Müns and coworkers, who investigated oxidative burst of neutrophils recovered from nasal lavage and blood of 24 patients with OSA (11). These authors measured the conversion rate of radiolabeled dihydrorhodamine elicited by incorporation of Escherichia coli bacteria by neutrophils. It was found that in OSA neither the number of blood neutrophils nor their oxidative burst activity was altered when compared with healthy controls. However, the test employed in this study delineates only the bactericidal activity of neutrophils, being unable to measure oxidative burst in response to other, i.e., nonbacterial stimuli. Furthermore, this method cannot directly quantify the concentrations of free oxygen radicals released from neutrophils.
To overcome these methodologic limitations, we aimed to determine the release of superoxide from circulating neutrophils of patients with OSA undergoing ex vivo challenge by the bacterial tripeptide formylmethionylleucylphenylalanine (fMLP) and the calcium ionophore A23. These substances represent well-established and powerful stimuli of superoxide production from neutrophils irrespective of the eventual trigger. Even more important, through measurement of superoxide dismutase-inhibitable reduction of cytochrome c, exact quantification of neutrophil superoxide generation is made possible (12).
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METHODS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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Patients
Eighteen consecutive patients with a polysomnographically verified diagnosis of OSA were investigated. Before participation, all patients had given informed written consent and the study protocol had been approved by the local ethics committee.
In all patients serum creatinine (normal, < 1.2 mg/dl), total cholesterol (normal, < 200 mg/dl), and fasting blood glucose levels (normal, < 110 mg/dl) were measured. Furthermore, peripheral white blood cell counts were determined (normal, 4-10 × 103/µl). The patients were asked about their regular medications and smoking habits. The medical history of each patient was evaluated with special reference to the presence of cardiovascular disease (i.e., arterial hypertension, coronary artery disease, and cerebrovascular disease). Blood pressure at rest was measured at fixed time intervals during the stay of the patients in the sleep laboratory (at 6:00 A.M., noon, 4:00 P.M., and 8:00 P.M.). Arterial hypertension was diagnosed if blood pressure values exceeded 140/90 mm Hg during at least two different measurements or if there was known and medically treated hypertension. Patients with ongoing systemic infection were excluded from the study.
Ten healthy nonsmoking volunteers were taken as the first control group (all males, mean age 30 ± 3 yr, body mass index [BMI] 22.9 ± 2.6 kg/m2). Ten patients without OSA and who were hospitalized because of lung cancer served as the second control group.
Among the control subjects, OSA was excluded by a negative history of sleep-related symptoms (i.e., snoring, witnessed apneas, excessive daytime sleepiness) and by overnight pulse oximetry recordings. The characteristics of the OSA group and the second control group are summarized in Table 1.
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Polysomnography
Polysomnography was performed on three consecutive nights. The electroencephalogram (electrodes at positions C3-A2 and C4-A1 of the international 10-20 system), electrooculogram, and electromyogram of the submandibular and pretibial muscles were simultaneously recorded. Ventilatory airflow at the nose and mouth was registered with thermistors. The breathing movements of the chest and abdomen were monitored by inductive plethysmography. The arterial oxygen saturation (SaO2) was measured transcutaneously with pulse oximetry at the finger tip of the patient. Finally, an electrocardiogram was obtained. All data were registered on a computerised polysomnograph with capability for analog registration (Sidas GS; IfM GmbH, Wettenberg, Germany). Analysis of sleep stages was performed manually at 30-s intervals according to the criteria of Rechtschaffen and Kales.
An obstructive apnea was diagnosed if complete cessation of oronasal flow occurred in the presence of thoracoabdominal breathing movements. If neither oronasal flow nor breathing efforts of the chest and abdomen could be detected this was scored as a central apnea. Hypopnea was defined as a reduction of the respiratory amplitude by greater than 50% with regard to the preceding effort signals.
All apneas and hypopneas were required to have a duration of at least 10 s. The apnea-hypopnea index (AHI) was obtained by dividing the total number of apneas and hypopneas through the total sleep time. An AHI of more than 10 per hour of sleep was considered as diagnostic of OSA.
During the first night a diagnostic study was performed. After the confirmation of the diagnosis of OSA, continuous positive airway pressure (CPAP) therapy was applied to all patients during the second night (Somnotron 4; Weinmann, Hamburg, Germany). Over the third night all patients slept with the final titrated pressure to assure adequate elimination of all apneas, hypopneas, and snoring.
After various times of CPAP use at home (range, 43-239 d), 10 of the 18 patients with OSA were reexamined in our sleep laboratory. Compliance with CPAP therapy was evaluated by the readings of the built-in time counter of the CPAP machine. Good compliance was defined as CPAP use for at least 5 h per night during 5 d of the week. During the control night, the adequacy of the initially chosen CPAP was checked. It was increased if snoring or apneas persisted; otherwise it was kept constant or decreased if possible.
Measurement of Superoxide Release from Neutrophils
Peripheral venous blood samples were obtained at 7:00 A.M. from the patients with OSA and the control subjects. In the patients with OSA this was done before and after the initiation of CPAP treatment (i.e., after the first two nights of CPAP therapy and at follow-up). Blood samples were withdrawn in EDTA-prepared tubes and immediately forwarded for neutrophil isolation.
Before isolation of polymorphonuclear neutrophils (PMNs), the EDTA-anticoagulated blood was centrifuged in a Ficoll-Paque (Pharmacia, Uppsala, Sweden) gradient, erythrocytes were sedimented with polyvinyl alcohol (Merck-Schuchardt, Hohenbrunn, Germany), and residual erythrocytes were removed by hypotonic lysis. Cells were washed twice (150 × g, 10 min, 4° C) and resuspended in phosphate-buffered saline (298 mM) with Ca2+ and Mg2+ (PBS) at a final concentration of 5 × 106/ml. Cell purity was > 98% (Pappenheim staining) and cell viability was > 96% (trypan blue exclusion) throughout.
Isolated PMNs were stimulated to produce superoxide anions
(O2
) by adding the bacterial tripeptide fMLP and the calcium ionophore A23 to the probes. O2 generation was measured as superoxide
dismutase-inhibitable reduction of cytochrome c as described (12).
Duplicate reaction mixtures containing PMNs (5 × 106/ml) and 75 µM ferricytochrome c were incubated at 37° C in the presence or absence of superoxide dismutase (10 µg/ml). PMN O2 production was
finally expressed as nanomoles of O2 per 5 × 106 PMNs.
Statistical Analysis
All data are given as means ± SEM. For comparison of superoxide release between the three different patient groups (OSA group, and
control groups 1 and 2), the Kruskal-Wallis test was employed. The
intergroup differences were then evaluated by the Dunn test, including an 
correction according to Holm.
Within the OSA group, the intraindividual differences between superoxide release before CPAP therapy, after two nights of CPAP therapy, and at follow-up were evaluated by the Friedman test. Subsequently, to control the familywise error rate, the Holm procedure as modified by Schafer was used.
Finally, it was tested if the superoxide concentrations were linearly correlated with the degree of nocturnal oxygen desaturation (as expressed as SaO2 < 90%, as a percentage of total sleep time) as well as the AHI. A p value of < 0.05 was considered to be significant.
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RESULTS |
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INTRODUCTION
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DISCUSSION
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Patient Characteristics
As shown in Table 1, the patients with OSA were on average 12 yr younger than the patients of the second control group. Furthermore, they were markedly obese, whereas the controls were not overweight. The peripheral white blood cell count was within the normal range for all patients. A high percentage of the patients with OSA and of the patients in control group 2 had hypercholesterolemia. All patients had normal serum creatinine concentrations and only two patients with OSA had mild diabetes mellitus. As the patients of the second control group all suffered from lung cancer, the percentage of smokers was higher than in the OSA group. The spectrum of cardiovascular morbidity was similar in both groups. As already mentioned, the first control group was composed of healthy nonsmoking young volunteers.
Polysomnographic Data
The patients with OSA had moderate to severe sleep-disordered breathing, with marked nocturnal oxygen desaturation and disturbed sleep architecture (Table 1). All patients were efficiently treated by nasal CPAP, with the mean pressure set at 10.0 ± 0.6 cm H2O. The mean duration of the follow-up period was 4.8 ± 0.6 mo. Of the 10 patients who were reevaluated after that time, there was no significant change in BMI, blood pressure, or blood parameters except for one patient, who had lost weight.
All patients had regularly used their CPAP device (average usage time, 5.4 ± 0.5 h per night). They reported improvement of daytime sleepiness and did not suffer from serious side effects of CPAP therapy. In the patient who had lost weight the CPAP pressure was reduced by 2 cm H2O, whereas in the remaining patients it was kept constant.
Superoxide Release before CPAP
The superoxide release in response to fMLP and A23 stimulation was lowest in the young healthy control group (3.7 ± 0.5 and 9.3 ± 1.5 nmol of O2 per 5 × 106 PMNs, respectively).
The other control group showed modestly higher superoxide
levels (4.1 ± 0.6 and 12.0 ± 1.4 nmol of O2 per 5 × 106
PMNs); however, these differences did not reach significance. In contrast, fMLP-stimulated superoxide release was markedly increased in the patients with untreated OSA when compared with both control groups (14.1 ± 1.5 nmol of O2 per 5 × 106 PMNs, p < 0.01 for each comparison; multiplicative factor,
3.4-3.8; Figure 1A). O2 production after stimulation with
A23 was also significantly elevated in OSA, but to a somewhat lesser extent (16.0 ± 1.1 nmol of O2 per 5 × 106 PMNs,
p = 0.01 when compared with control group 1 and p = 0.05 when compared with control group 2; multiplicative factor,
1.4-2.1; Figure 1B). The superoxide levels were not different
between OSA patients with and without cardiovascular disease (fMLP, 13.6 ± 2.6 versus 14.1 ± 2.1 nmol of O2 per 5 × 106 PMNs; A23, 16.4 ± 1.4 versus 15.9 ± 1.7 nmol of O2 per
5 × 106 PMNs; data not shown).
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0.05, **p The same was true for patients with and without hypercholesterolemia (fMLP, 13.8 ± 1.7 versus 15.0 ± 3.9 nmol of O2
per 5 × 106 PMNs; A23, 16.4 ± 1.2 versus 16.0 ± 2.5 nmol of
O2 per 5 × 106 PMNs; data not shown). When looking at individual data, there was virtually no overlap between the OSA
group and the control groups with regard to fMLP-elicited superoxide release (only two patients with OSA had O2 concentrations comparable to the highest levels measured in the control subjects). In contrast, superoxide release in response to A23 showed a significant overlap of single values between
OSA and non-OSA patients. Superoxide levels in OSA were
weakly correlated with the degree of nocturnal oxygen desaturation (r = 0.42) and the AHI (r = 0.38); however, this was not significant.
Superoxide Release after CPAP
After only two nights of CPAP therapy, superoxide release
was reduced in almost all patients with OSA. When compared
with the data obtained before CPAP initiation, superoxide
generation in response to fMLP challenge was reduced by
43% (to 8.1 ± 1.5 nmol of O2 per 5 × 106 PMNs, p < 0.01;
Figure 2A) and to A23 challenge by 16% (to 13.7 ± 1.1 nmol
of O2 per 5 × 106 PMNs, p = NS; Figure 2B). At follow-up,
the superoxide concentrations were further reduced to levels
now comparable to those of both control groups (fMLP, 5.5 ± 0.6 nmol of O2 per 5 × 106 PMNs; A23, 11.0 ± 2.3 nmol of
O2 per 5 × 106 PMNs). The average reduction in superoxide
concentrations with regard to the pre-CPAP values was 61%
after fMLP (p < 0.01) and 33% after A23 (p = 0.05).
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In two healthy volunteers, superoxide release was also measured after a night with CPAP set a pressure of 8 cm H2O. In these subjects, no significant change in superoxide production was observed after CPAP application.
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DISCUSSION |
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ABSTRACT
INTRODUCTION
METHODS
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Among subjects with untreated OSA the release of superoxide from circulating neutrophils was markedly enhanced when compared with the control subjects. After only two nights of CPAP therapy superoxide release was significantly reduced in almost all patients with OSA. Continuous CPAP therapy even resulted in near-normal levels of superoxide release in the OSA patients with long-term follow-up.
Before discussing these observations, one might wonder why there was virtually no difference between superoxide levels in the control groups. First, this might be due to compartmentalized neutrophil activation in control group 2. Smoking, chronic bronchitis, and lung cancer will primarily lead to neutrophil activation within the airways and the lungs, which will not be evident when measuring superoxide release from circulating neutrophils (13). Second, when considering the impact of cardiovascular disease on superoxide generation from neutrophils, the activity of the disease process is of major importance. Only in unstable angina, myocardial infarction, and uncontrolled hypertension has the oxidative burst of blood neutrophils been found to be significantly enhanced (8, 9, 16, 17). If there is no persistent myocardial ischemia and if blood pressure is adequately regulated by antihypertensive drugs, as was the case for the patients of control group 2, intravascular oxidative stress can be expected to be low.
In comparison with both control groups, the patients with OSA were characterized by markedly enhanced neutrophil superoxide generation. This and the rapid decline in neutrophil superoxide release on onset of CPAP therapy clearly deny the view that differences in underlying morbidity might be responsible for the widely divergent superoxide production in non-OSA and OSA patients. A final argument for the validity of our results is the fact that, in contrast to the patients with OSA, CPAP therapy had no significant impact on superoxide release in two healthy volunteers undergoing a night of CPAP ventilation.
In contrast to our own findings, in the earlier study by Müns and coworkers the neutrophil oxidative burst was not increased in OSA (11). Apart from the already mentioned methodologic limitations of this study, it might be possible that a bias resulted from the time of blood sampling. Müns and colleagues did not state at which time they obtained the blood specimens. However, if blood was not withdrawn in the morning shortly after awakening, the oxidative burst might erroneously have been determined to lie in the normal range. In our study measurements of superoxide release from neutrophils were carried out at 7:00 A.M. throughout, i.e., at a time when the cells had just been exposed to apnea-related hypoxemia.
In our opinion it is unlikely that the enhanced release of superoxide from circulating neutrophils is due to local activation of these cells in the upper airway mucosa of patients with OSA. First of all, there is no real mucosal inflammation in OSA but merely mechanical irritation, which presumably will not lead to activation of leukocytes. Furthermore, if neutrophil bursting occurs in the pharyngeal tissue this phenomenon will remain localized and not be evident when measuring release of radicals from cells derived from the systemic circulation.
The present study did not address the signaling events underlying the enhanced readiness of neutrophils from patients with OSA to respond with superoxide generation. It is interesting that the phenomenon was observed for both fMLP- and calcium ionophore challenge; however, the differences were more prominent for the ligand-mediated stimulation. This finding may suggest changes in the upstream signaling cascade in the neutrophils rather than changes in the leukocyte NADPH oxidase itself as underlying mechanism(s).
"Priming" of neutrophils is known to occur on in vivo and in vitro incubation with lipopolysaccharides or proinflammatory cytokines, resulting in enhanced responsiveness including respiratory burst to a second inflammatory challenge (18). We are not aware of any study addressing whether such priming might also be provoked by periodic changes in oxygen or carbon dioxide tensions, as occurs under conditions of OSA. The fact that superoxide concentrations were not significantly related to the degree of nocturnal oxygen desaturation argues against blood gas alterations as the primary triggers of superoxide generation in OSA. Alternatively, mediators secondarily arising in the patients with OSA might be involved in neutrophil priming. Two of these substances are tumor necrosis factor and interleukin 6, which are potent triggers of radical release from PMNs and that have been reported to be elevated in OSA (19, 20). Regardless of the mechanism(s) involved, the alteration of the leukocyte responsiveness does, however, clearly occur in vivo and is not "transported" by the plasma fraction in the blood sample, as the neutrophils were isolated from the other blood constituents before undergoing ionophore or fMLP challenge.
The presently observed neutrophil priming for an enhanced respiratory burst might well be related to pathophysiological sequelae occurring in patients with OSA. The increased superoxide release might induce the expression of vascular adhesion molecules, the proliferation of vascular smooth muscle cells, and the aggregation and activation of platelets (21). In addition, low-density lipoprotein (LDL) cholesterol is oxidized under the influence of superoxide and incorporated into macrophages, thus forming foam cells (24). Finally, nitric oxide, the main vasodilator released from the endothelium, is broken down to peroxynitrite (25). All these events have been implicated in the pathogenesis of atherosclerosis, known to take place with enhanced rapidity in OSA, and at least some of them have already been described in these patients (26).
CPAP therapy has been shown to have beneficial effects on long-term survival of patients with OSA (2). The rapid and long-lasting reduction in superoxide release from neutrophils after the institution of CPAP might constitute one mechanism through which this form of therapy prevents the development and progression of cardiovascular morbidity and mortality in OSA.
In conclusion, markedly enhanced readiness of neutrophils to respond with superoxide generation to different stimuli was noted in patients with OSA, rapidly reversible on onset of CPAP therapy. The exact mechanisms underlying such "priming" of neutrophils for enhanced respiratory burst under conditions of OSA remain to be further elucidated. However, this finding may be relevant to the increased cardiovascular morbidity observed in patients with OSA. Furthermore, CPAP therapy, by reducing this oxidative stress both in the short and long term, might prevent the emergence and progression of cardiovascular disease in OSA.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Richard Schulz, M.D., Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Justus-Liebig-University, Klinikstr. 36, 35392 Giessen, Germany.
(Received in original form August 20, 1999 and in revised form January 31, 2000).
This work contains parts of the doctoral thesis of S. Mahmoudi.Acknowledgments: Supported by a grant from Weinmann, Inc. (Hamburg, Germany).
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References |
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 A Alonso-Fernandez, F Garcia-Rio, M A Arias, A Hernanz, M de la Pena, J Pierola, A Barcelo, E Lopez-Collazo, and A Agusti Effects of CPAP on oxidative stress and nitrate efficiency in sleep apnoea: a randomised trial Thorax, July 1, 2009; 64(7): 581 - 586. [Abstract] [Full Text] [PDF]
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 L. Lavie and P. Lavie Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link Eur. Respir. J., June 1, 2009; 33(6): 1467 - 1484. [Abstract] [Full Text] [PDF]
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 U. Kuhlmann, F. G. Bormann, and H. F. Becker Obstructive sleep apnoea: clinical signs, diagnosis and treatment Nephrol. Dial. Transplant., January 1, 2009; 24(1): 8 - 14. [Full Text] [PDF]
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 R. M. Douglas and G. G. Haddad Can O2 Dysregulation Induce Premature Aging? Physiology, December 1, 2008; 23(6): 333 - 349. [Abstract] [Full Text] [PDF]
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P. Levy, J-L. Pepin, C. Arnaud, R. Tamisier, J-C. Borel, M. Dematteis, D. Godin-Ribuot, and C. Ribuot Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives Eur. Respir. J., October 1, 2008; 32(4): 1082 - 1095. [Abstract] [Full Text] [PDF]
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 J. Jun, V. Savransky, A. Nanayakkara, S. Bevans, J. Li, P. L. Smith, and V. Y. Polotsky Intermittent hypoxia has organ-specific effects on oxidative stress Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2008; 295(4): R1274 - R1281. [Abstract] [Full Text] [PDF]
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 V. K. Somers, D. P. White, R. Amin, W. T. Abraham, F. Costa, A. Culebras, S. Daniels, J. S. Floras, C. E. Hunt, L. J. Olson, et al. Sleep Apnea and Cardiovascular Disease: An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health) Circulation, September 2, 2008; 118(10): 1080 - 1111. [Full Text] [PDF]
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V. K. Somers, D. P. White, R. Amin, W. T. Abraham, F. Costa, A. Culebras, S. Daniels, J. S. Floras, C. E. Hunt, L. J. Olson, et al. Sleep Apnea and Cardiovascular Disease: An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health) J. Am. Coll. Cardiol., August 19, 2008; 52(8): 686 - 717. [Full Text] [PDF]
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B. Lefebvre, J-L. Pepin, J-P. Baguet, R. Tamisier, M. Roustit, K. Riedweg, G. Bessard, P. Levy, and F. Stanke-Labesque Leukotriene B4: early mediator of atherosclerosis in obstructive sleep apnoea? Eur. Respir. J., July 1, 2008; 32(1): 113 - 120. [Abstract] [Full Text] [PDF]
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P. Faure, R. Tamisier, J-P. Baguet, A. Favier, S. Halimi, P. Levy, and J-L. Pepin Impairment of serum albumin antioxidant properties in obstructive sleep apnoea syndrome Eur. Respir. J., May 1, 2008; 31(5): 1046 - 1053. [Abstract] [Full Text] [PDF]
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S. Jelic, M. Padeletti, S. M. Kawut, C. Higgins, S. M. Canfield, D. Onat, P. C. Colombo, R. C. Basner, P. Factor, and T. H. LeJemtel Inflammation, Oxidative Stress, and Repair Capacity of the Vascular Endothelium in Obstructive Sleep Apnea Circulation, April 29, 2008; 117(17): 2270 - 2278. [Abstract] [Full Text] [PDF]
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 M. H. Sanders, J. M. Montserrat, R. Farre, and R. J. Givelber Positive Pressure Therapy: A Perspective on Evidence-based Outcomes and Methods of Application Proceedings of the ATS, February 15, 2008; 5(2): 161 - 172. [Abstract] [Full Text] [PDF]
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J. M. Golbin, V. K. Somers, and S. M. Caples Obstructive Sleep Apnea, Cardiovascular Disease, and Pulmonary Hypertension Proceedings of the ATS, February 15, 2008; 5(2): 200 - 206. [Abstract] [Full Text] [PDF]
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E. Tasali and M. S. M. Ip Obstructive Sleep Apnea and Metabolic Syndrome: Alterations in Glucose Metabolism and Inflammation Proceedings of the ATS, February 15, 2008; 5(2): 207 - 217. [Abstract] [Full Text] [PDF]
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D. Gozal and L. Kheirandish-Gozal Cardiovascular Morbidity in Obstructive Sleep Apnea: Oxidative Stress, Inflammation, and Much More Am. J. Respir. Crit. Care Med., February 15, 2008; 177(4): 369 - 375. [Abstract] [Full Text] [PDF]
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 L. Kheirandish-Gozal, O. Sans Capdevila, E. Kheirandish, and D. Gozal Elevated Serum Aminotransferase Levels in Children at Risk for Obstructive Sleep Apnea Chest, January 1, 2008; 133(1): 92 - 99. [Abstract] [Full Text] [PDF]
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 B. Buyse, J. Hedner, and the participants of working group 2 Sleep apnoea, hypertension and vascular disease: where are we now? Eur. Respir. Rev., December 1, 2007; 16(106): 169 - 182. [Abstract] [Full Text] [PDF]
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 C. Selmi, N. Montano, R. Furlan, C. L. Keen, and M. E. Gershwin Inflammation and Oxidative Stress in Obstructive Sleep Apnea Syndrome Exp Biol Med, December 1, 2007; 232(11): 1409 - 1413. [Abstract] [Full Text] [PDF]
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F. Campos-Rodriguez, J. Perez-Ronchel, A. Grilo-Reina, J. Lima-Alvarez, M. A. Benitez, and C. Almeida-Gonzalez Long-term Effect of Continuous Positive Airway Pressure on BP in Patients With Hypertension and Sleep Apnea Chest, December 1, 2007; 132(6): 1847 - 1852. [Abstract] [Full Text] [PDF]
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E. Barreiro, A. Nowinski, J. Gea, and P. Sliwinski Oxidative stress in the external intercostal muscles of patients with obstructive sleep apnoea Thorax, December 1, 2007; 62(12): 1095 - 1101. [Abstract] [Full Text] [PDF]
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 V. Savransky, S. Bevans, A. Nanayakkara, J. Li, P. L. Smith, M. S. Torbenson, and V. Y. Polotsky Chronic intermittent hypoxia causes hepatitis in a mouse model of diet-induced fatty liver Am J Physiol Gastrointest Liver Physiol, October 1, 2007; 293(4): G871 - G877. [Abstract] [Full Text] [PDF]
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G. Parati, C. Lombardi, and K. Narkiewicz Sleep apnea: epidemiology, pathophysiology, and relation to cardiovascular risk Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2007; 293(4): R1671 - R1683. [Abstract] [Full Text] [PDF]
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R. K. Kakkar and R. B. Berry Positive Airway Pressure Treatment for Obstructive Sleep Apnea Chest, September 1, 2007; 132(3): 1057 - 1072. [Abstract] [Full Text] [PDF]
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A. A. El Solh, M. E. Akinnusi, F. H. Baddoura, and C. R. Mankowski Endothelial Cell Apoptosis in Obstructive Sleep Apnea: A Link to Endothelial Dysfunction Am. J. Respir. Crit. Care Med., June 1, 2007; 175(11): 1186 - 1191. [Abstract] [Full Text] [PDF]
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T. H. Le Jemtel and S. Jelic Seek and Treat Obstructive Sleep Apnea in Heart Failure J. Am. Coll. Cardiol., April 17, 2007; 49(15): 1632 - 1633. [Full Text] [PDF]
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H. Wang, J. D. Parker, G. E. Newton, J. S. Floras, S. Mak, K.-L. Chiu, P. Ruttanaumpawan, G. Tomlinson, and T. D. Bradley Influence of Obstructive Sleep Apnea on Mortality in Patients With Heart Failure J. Am. Coll. Cardiol., April 17, 2007; 49(15): 1625 - 1631. [Abstract] [Full Text] [PDF]
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G. E. Foster, P. J. Hanly, M. Ostrowski, and M. J. Poulin Effects of Continuous Positive Airway Pressure on Cerebral Vascular Response to Hypoxia in Patients with Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., April 1, 2007; 175(7): 720 - 725. [Abstract] [Full Text] [PDF]
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S. Itzhaki, H. Dorchin, G. Clark, L. Lavie, P. Lavie, and G. Pillar The Effects of 1-Year Treatment With a Herbst Mandibular Advancement Splint on Obstructive Sleep Apnea, Oxidative Stress, and Endothelial Function Chest, March 1, 2007; 131(3): 740 - 749. [Abstract] [Full Text] [PDF]
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R. M. Douglas, N. Miyasaka, K. Takahashi, A. Latuszek-Barrantes, G. G. Haddad, and H. P. Hetherington Chronic intermittent but not constant hypoxia decreases NAA/Cr ratios in neonatal mouse hippocampus and thalamus Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1254 - R1259. [Abstract] [Full Text] [PDF]
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W. T. McNicholas, M. R. Bonsignore, and the Management Committee of EU COST ACTION B26 Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities Eur. Respir. J., January 1, 2007; 29(1): 156 - 178. [Abstract] [Full Text] [PDF]
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 R. Wolk and V. K. Somers Sleep Apnoea & Hypertension: Physiological bases for a causal relation: Sleep and the metabolic syndrome Exp Physiol, January 1, 2007; 92(1): 67 - 78. [Abstract] [Full Text] [PDF]
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G. E. Foster, M. J. Poulin, and P. J. Hanly Sleep Apnoea & Hypertension: Physiological bases for a causal relation: Intermittent hypoxia and vascular function: implications for obstructive sleep apnoea Exp Physiol, January 1, 2007; 92(1): 51 - 65. [Abstract] [Full Text] [PDF]
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K. Minoguchi, T. Yokoe, A. Tanaka, S. Ohta, T. Hirano, G. Yoshino, C. P. O'Donnell, and M. Adachi Association between lipid peroxidation and inflammation in obstructive sleep apnoea. Eur. Respir. J., August 1, 2006; 28(2): 378 - 385. [Abstract] [Full Text] [PDF]
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 K Palombi, E Renard, P Levy, C Chiquet, C. Deschaux, J P Romanet, and J L Pepin Non-arteritic anterior ischaemic optic neuropathy is nearly systematically associated with obstructive sleep apnoea Br J Ophthalmol, July 1, 2006; 90(7): 879 - 882. [Abstract] [Full Text] [PDF]
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F. Campos-Rodriguez, A. Grilo-Reina, J. Perez-Ronchel, M. Merino-Sanchez, M. A. Gonzalez-Benitez, M. Beltran-Robles, and C. Almeida-Gonzalez Effect of Continuous Positive Airway Pressure on Ambulatory BP in Patients With Sleep Apnea and Hypertension: A Placebo-Controlled Trial Chest, June 1, 2006; 129(6): 1459 - 1467. [Abstract] [Full Text] [PDF]
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M. Grebe, H. J. Eisele, N. Weissmann, C. Schaefer, H. Tillmanns, W. Seeger, and R. Schulz Antioxidant Vitamin C Improves Endothelial Function in Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., April 15, 2006; 173(8): 897 - 901. [Abstract] [Full Text] [PDF]
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C. L. Phillips and R. R. Grunstein Obstructive sleep apnoea: time for a radical change? Eur. Respir. J., April 1, 2006; 27(4): 671 - 673. [Full Text] [PDF]
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A. Barcelo, F. Barbe, M. de la Pena, M. Vila, G. Perez, J. Pierola, J. Duran, and A. G. N. Agusti Antioxidant status in patients with sleep apnoea and impact of continuous positive airway pressure treatment. Eur. Respir. J., April 1, 2006; 27(4): 756 - 760. [Abstract] [Full Text] [PDF]
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L. M. O'Brien, L. D. Serpero, R. Tauman, and D. Gozal Plasma adhesion molecules in children with sleep-disordered breathing. Chest, April 1, 2006; 129(4): 947 - 953. [Abstract] [Full Text] [PDF]
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 A. Svatikova, R. Wolk, L. O. Lerman, L. A. Juncos, E. L. Greene, J. P. McConnell, and V. K. Somers Oxidative stress in obstructive sleep apnoea Eur. Heart J., November 2, 2005; 26(22): 2435 - 2439. [Abstract] [Full Text] [PDF]
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 L J Cormican and A Williams Sleep disordered breathing and its treatment in congestive heart failure Heart, October 1, 2005; 91(10): 1265 - 1270. [Abstract] [Full Text] [PDF]
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L. Chen, E. Einbinder, Q. Zhang, J. Hasday, C. W. Balke, and S. M. Scharf Oxidative Stress and Left Ventricular Function with Chronic Intermittent Hypoxia in Rats Am. J. Respir. Crit. Care Med., October 1, 2005; 172(7): 915 - 920. [Abstract] [Full Text] [PDF]
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G. Zhan, F. Serrano, P. Fenik, R. Hsu, L. Kong, D. Pratico, E. Klann, and S. C. Veasey NADPH Oxidase Mediates Hypersomnolence and Brain Oxidative Injury in a Murine Model of Sleep Apnea Am. J. Respir. Crit. Care Med., October 1, 2005; 172(7): 921 - 929. [Abstract] [Full Text] [PDF]
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K. Minoguchi, T. Yokoe, T. Tazaki, H. Minoguchi, A. Tanaka, N. Oda, S. Okada, S. Ohta, H. Naito, and M. Adachi Increased Carotid Intima-Media Thickness and Serum Inflammatory Markers in Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., September 1, 2005; 172(5): 625 - 630. [Abstract] [Full Text] [PDF]
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 G. E. Foster, D. C. McKenzie, W. K. Milsom, and A. W. Sheel Effects of two protocols of intermittent hypoxia on human ventilatory, cardiovascular and cerebral responses to hypoxia J. Physiol., September 1, 2005; 567(2): 689 - 699. [Abstract] [Full Text] [PDF]
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R. Schulz The vascular micromilieu in obstructive sleep apnoea Eur. Respir. J., May 1, 2005; 25(5): 780 - 782. [Full Text] [PDF]
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M. Yamauchi, H. Nakano, J. Maekawa, Y. Okamoto, Y. Ohnishi, T. Suzuki, and H. Kimura Oxidative Stress in Obstructive Sleep Apnea Chest, May 1, 2005; 127(5): 1674 - 1679. [Abstract] [Full Text] [PDF]
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 M. Joyeux-Faure, F. Stanke-Labesque, B. Lefebvre, P. Beguin, D. Godin-Ribuot, C. Ribuot, S. H. Launois, G. Bessard, and P. Levy Chronic intermittent hypoxia increases infarction in the isolated rat heart J Appl Physiol, May 1, 2005; 98(5): 1691 - 1696. [Abstract] [Full Text] [PDF]
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A. G. Kaditis, E. I. Alexopoulos, E. Kalampouka, E. Kostadima, A. Germenis, E. Zintzaras, and K. Gourgoulianis Morning Levels of C-Reactive Protein in Children with Obstructive Sleep-disordered Breathing Am. J. Respir. Crit. Care Med., February 1, 2005; 171(3): 282 - 286. [Abstract] [Full Text] [PDF]
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R. Schulz, W. Seeger, C. Fegbeutel, H. Husken, R. H. Bodeker, H. Tillmanns, and M. Grebe Changes in extracranial arteries in obstructive sleep apnoea Eur. Respir. J., January 1, 2005; 25(1): 69 - 74. [Abstract] [Full Text] [PDF]
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T. Tazaki, K. Minoguchi, T. Yokoe, K. T. R. Samson, H. Minoguchi, A. Tanaka, Y. Watanabe, and M. Adachi Increased Levels and Activity of Matrix Metalloproteinase-9 in Obstructive Sleep Apnea Syndrome Am. J. Respir. Crit. Care Med., December 15, 2004; 170(12): 1354 - 1359. [Abstract] [Full Text] [PDF]
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A.G. Kaditis, E.I. Alexopoulos, E. Kalampouka, E. Kostadima, N. Angelopoulos, A. Germenis, E. Zintzaras, and K. Gourgoulianis Morning levels of fibrinogen in children with sleep-disordered breathing Eur. Respir. J., November 1, 2004; 24(5): 790 - 797. [Abstract] [Full Text] [PDF]
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K. Minoguchi, T. Tazaki, T. Yokoe, H. Minoguchi, Y. Watanabe, M. Yamamoto, and M. Adachi Elevated Production of Tumor Necrosis Factor-{alpha} by Monocytes in Patients With Obstructive Sleep Apnea Syndrome Chest, November 1, 2004; 126(5): 1473 - 1479. [Abstract] [Full Text] [PDF]
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A. Svatikova, R. Wolk, H. H. Wang, M. E. Otto, K. A. Bybee, R. J. Singh, and V. K. Somers Circulating free nitrotyrosine in obstructive sleep apnea Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2004; 287(2): R284 - R287. [Abstract] [Full Text] [PDF]
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 J. M. Parish and V. K. Somers Obstructive Sleep Apnea and Cardiovascular Disease Mayo Clin. Proc., August 1, 2004; 79(8): 1036 - 1046. [Abstract] [PDF]
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U. Hatipoglu and I. Rubinstein Inflammation and Obstructive Sleep Apnea Syndrome: How Many Ways Do I Look at Thee? Chest, July 1, 2004; 126(1): 1 - 2. [Full Text] [PDF]
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G J Gibson Sleep disordered breathing and the outcome of stroke Thorax, May 1, 2004; 59(5): 361 - 363. [Full Text] [PDF]
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S. F. Quan and B. J. Gersh Cardiovascular Consequences of Sleep-Disordered Breathing: Past, Present and Future: Report of a Workshop From the National Center on Sleep Disorders Research and the National Heart, Lung, and Blood Institute Circulation, March 2, 2004; 109(8): 951 - 957. [Full Text] [PDF]
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T. Altay, E. R. Gonzales, T. S. Park, and J. M. Gidday Cerebrovascular inflammation after brief episodic hypoxia: modulation by neuronal and endothelial nitric oxide synthase J Appl Physiol, March 1, 2004; 96(3): 1223 - 1230. [Abstract] [Full Text] [PDF]
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S. Javaheri, W. T. Abraham, C. Brown, H. Nishiyama, R. Giesting, and L. E. Wagoner Prevalence of obstructive sleep apnoea and periodic limb movement in 45 subjects with heart transplantation Eur. Heart J., February 1, 2004; 25(3): 260 - 266. [Abstract] [Full Text] [PDF]
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M. S. M. Ip, H.-F. Tse, B. Lam, K. W. T. Tsang, and W.-K. Lam Endothelial Function in Obstructive Sleep Apnea and Response to Treatment Am. J. Respir. Crit. Care Med., February 1, 2004; 169(3): 348 - 353. [Abstract] [Full Text] [PDF]
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P. Lavie Pro: Sleep Apnea Causes Cardiovascular Disease Am. J. Respir. Crit. Care Med., January 15, 2004; 169(2): 147 - 148. [Full Text] [PDF]
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 R. Wolk, A. S.M. Shamsuzzaman, and V. K. Somers Obesity, Sleep Apnea, and Hypertension Hypertension, December 1, 2003; 42(6): 1067 - 1074. [Abstract] [Full Text] [PDF]
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 A. S. M. Shamsuzzaman, B. J. Gersh, and V. K. Somers Obstructive Sleep Apnea: Implications for Cardiac and Vascular Disease JAMA, October 8, 2003; 290(14): 1906 - 1914. [Abstract] [Full Text] [PDF]
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G. E. Carpagnano, S. A. Kharitonov, O. Resta, M. P. Foschino-Barbaro, E. Gramiccioni, and P. J. Barnes 8-Isoprostane, a Marker of Oxidative Stress, Is Increased in Exhaled Breath Condensate of Patients With Obstructive Sleep Apnea After Night and Is Reduced by Continuous Positive Airway Pressure Therapy Chest, October 1, 2003; 124(4): 1386 - 1392. [Abstract] [Full Text] [PDF]
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M. Hayashi, K. Fujimoto, K. Urushibata, S.-i. Uchikawa, H. Imamura, and K. Kubo Nocturnal Oxygen Desaturation Correlates With the Severity of Coronary Atherosclerosis in Coronary Artery Disease Chest, September 1, 2003; 124(3): 936 - 941. [Abstract] [Full Text] [PDF]
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Y.-J. Peng and N. R. Prabhakar Reactive oxygen species in the plasticity of respiratory behavior elicited by chronic intermittent hypoxia J Appl Physiol, June 1, 2003; 94(6): 2342 - 2349. [Abstract] [Full Text] [PDF]
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T. D. Bradley and J. S. Floras Sleep Apnea and Heart Failure: Part I: Obstructive Sleep Apnea Circulation, April 1, 2003; 107(12): 1671 - 1678. [Full Text] [PDF]
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T. Yokoe, K. Minoguchi, H. Matsuo, N. Oda, H. Minoguchi, G. Yoshino, T. Hirano, and M. Adachi Elevated Levels of C-Reactive Protein and Interleukin-6 in Patients With Obstructive Sleep Apnea Syndrome Are Decreased by Nasal Continuous Positive Airway Pressure Circulation, March 4, 2003; 107(8): 1129 - 1134. [Abstract] [Full Text] [PDF]
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G. E. Carpagnano, S. A. Kharitonov, O. Resta, M. P. Foschino-Barbaro, E. Gramiccioni, and P. J. Barnes Increased 8-Isoprostane and Interleukin-6 in Breath Condensate of Obstructive Sleep Apnea Patients Chest, October 1, 2002; 122(4): 1162 - 1167. [Abstract] [Full Text] [PDF]
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N. R. Prabhakar Sleep Apneas . An Oxidative Stress? Am. J. Respir. Crit. Care Med., April 1, 2002; 165(7): 859 - 860. [Full Text] [PDF]
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L. DYUGOVSKAYA, P. LAVIE, and L. LAVIE Increased Adhesion Molecules Expression and Production of Reactive Oxygen Species in Leukocytes of Sleep Apnea Patients Am. J. Respir. Crit. Care Med., April 1, 2002; 165(7): 934 - 939. [Abstract] [Full Text] [PDF]
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R. SCHULZ, C. HUMMEL, S. HEINEMANN, W. SEEGER, and F. GRIMMINGER Serum Levels of Vascular Endothelial Growth Factor Are Elevated in Patients with Obstructive Sleep Apnea and Severe Nighttime Hypoxia Am. J. Respir. Crit. Care Med., January 1, 2002; 165(1): 67 - 70. [Abstract] [Full Text] [PDF]
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W. Droge Free Radicals in the Physiological Control of Cell Function Physiol Rev, January 1, 2002; 82(1): 47 - 95. [Abstract] [Full Text] [PDF]
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R. S. T. LEUNG and T. DOUGLAS BRADLEY Sleep Apnea and Cardiovascular Disease Am. J. Respir. Crit. Care Med., December 15, 2001; 164(12): 2147 - 2165. [Full Text] [PDF]
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M. J. TOBIN Sleep-disordered Breathing, Control of Breathing, Respiratory Muscles, Pulmonary Function Testing, Nitric Oxide, and Bronchoscopy in AJRCCM 2000 Am. J. Respir. Crit. Care Med., October 15, 2001; 164(8): 1362 - 1375. [Full Text] [PDF]
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L. Lavie, A. Perelman, and P. Lavie Plasma Homocysteine Levels in Obstructive Sleep Apnea : Association With Cardiovascular Morbidity Chest, September 1, 2001; 120(3): 900 - 908. [Abstract] [Full Text] [PDF]
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R Schulz, D Schmidt, A Blum, X Lopes-Ribeiro, C Lücke, K Mayer, H Olschewski, W Seeger, and F Grimminger Decreased plasma levels of nitric oxide derivatives in obstructive sleep apnoea: response to CPAP therapy Thorax, December 1, 2000; 55(12): 1046 - 1051. [Abstract] [Full Text]
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