Published ahead of print on January 6, 2003, doi:10.1164/rccm.200201-057OC Am. J. Respir. Crit. Care Med., Volume 167, Number 6, March 2003, 895-901 A more recent version of this article appeared on March 15, 2003
Submitted on January 30, 2002 Inhaled NO Modifies LV Diastolic Stress in the Presence of Vasoactive Agents in Heart FailureShunsuke Natori1*,1 First Department of Internal Medicine, Asahikawa Medical College, Asahikawa, Hokkaido, Japan, 2 Department of Medical Electronics, Suzuka University of Medical Science and Technology, Suzuka, Mie, Japan * To whom correspondence should be addressed. E-mail: natoshun{at}pop07.odn.ne.jp.
Nitric oxide (NO) inhalation therapy has been widely used in several diseases with pulmonary hypertension. However, application of NO inhalation therapy remains controversial in heart failure. Cardiovascular effects of inhaled NO were evaluated in dogs before and after induction of heart failure with and without infusion of vasoactive agents. Inhaled NO did not affect the baseline left ventricular (LV) function or the response to isoproterenol in Control or heart failure induced by procainamide. Pulmonary vascular resistance was significantly decreased by inhaled NO in heart failure with infusion of vasoactive agents. Unexpectedly, LV end diastolic pressure was significantly elevated by inhaled NO in heart failure in the presence of infusion of vasoactive agents independent of their types; either the vasodilating agents of acetylcholine and nitroglycerin, or the vasoconstricting agents of norepinephrine and angiotensin-II. The end diastolic LV dimension and wall stress were also significantly increased by inhaled NO, however, those at end systole were not affected. These results suggested that NO inhalation therapy reduced pulmonary vascular resistance, whereas in the presence of additional stress of vasoactive agents, it increased LV preload and end diastolic wall stress in heart failure. Key words: nitric oxide, heart failure, cardiac output, hemodynamics. vasodilation
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