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Published ahead of print on November 9, 2006, doi:10.1164/rccm.200608-1199OC

Am. J. Respir. Crit. Care Med., Volume 175, Number 3, February 2007, 277-281

A more recent version of this article appeared on February 1, 2007
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Submitted on August 23, 2006
Accepted on November 8, 2006

Effects of Acetazolamide on Ventilation, Cerebrovascular and Pulmonary Vascular Responses to Hypoxia

Luc J Teppema1, George M Balanos2, Craig D Steinback3, Allison D Brown3, Glen E Foster3, Henry J Duff4, Richard Leigh4, and Marc J Poulin5*

1 Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands, 2 School of Sport and Exercise Sciences, University of Birmingham, Birmingham, United Kingdom, 3 Faculty of Medicine, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada, 4 Faculty of Medicine, Department of Medicine, University of Calgary, Calgary, Alberta, Canada, 5 Faculty of Medicine, Department of Medicine, University of Calgary, Calgary, Alberta, Canada; Faculty of Medicine, Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada; Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada

* To whom correspondence should be addressed. E-mail: poulin{at}ucalgary.ca.

Rationale: Acute Mountain Sickness (AMS) may affect individuals who (rapidly) ascend to altitudes higher than 2000-3000m. A more serious consequence of rapid ascent may be High Altitude Pulmonary Edema (HAPE), a hydrostatic edema associated with increased pulmonary capillary pressures. Acetazolamide is effective against AMS, possibly by increasing ventilation and cerebral blood flow (CBF). In animals it inhibits hypoxic pulmonary vasoconstriction. Objectives: We examined the influence of acetazolamide on the response to hypoxia of ventilation, CBF and pulmonary vascular resistance (PVR). Methods: In this double-blind placebo-controlled randomized study, nine subjects ingested 250 mg acetazolamide every 8 hours for three days. On the fourth test day we measured the responses of ventilation, PVR and CBF to acute isocapnic hypoxia (20 min) and sustained poikilocapnic hypoxia (4 hr). Ventilation was measured with pneumotachography. Hypoxia was achieved with dynamic end-tidal forcing. The maximum pressure difference across the tricuspid valve ({Delta}Pmax, a good index of PVR) was measured with Doppler echocardiography. CBF was measured by transcranial Doppler ultrasound. Results: In normoxia, acetazolamide increased ventilation and reduced {Delta}Pmax, but did not influence CBF. The ventilatory and CBF responses to acute isocapnic hypoxia were unaltered, but the rise in {Delta}Pmax was reduced by 57%. The increase in {Delta}Pmax by sustained poikilocapnic hypoxia observed after placebo was reduced by 34% after acetazolamide, the ventilatory response was increased, but the CBF response remained unaltered. Conclusions: Acetazolamide has complex effects on ventilation, PVR and CBF that converge to optimize brain oxygenation and may be a valuable means to prevent/treat HAPE.
Key words: pulmonary resistance, cerebral blood flow, altitude sickness, hypoxic responses, mountaineering




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