[abstract] MECHANISM OF PULMONARY HYPERTENSION IN CHRONIC HYPOXIA.

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[abstract] MECHANISM OF PULMONARY HYPERTENSION IN CHRONIC HYPOXIA.

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Title: [abstract] MECHANISM OF PULMONARY HYPERTENSION IN CHRONIC HYPOXIA.
Author: Chen, SY; Huang, KL; Kang, BH; Wan, FJ
Abstract: INTRODUCTION: Hypoxia accounts for the pulmonary hypertension in people living at high altitude. Since the pathogenesis of hypoxic pulmonary hypertension remains under widely investigated, the management is still an invincible difficulty for the clinicians. Disruptions in the nitric oxide pathway have been implicated in the pathogenesis of hypoxia- induced pulmonary hypertension. However, the increase or decrease of NO production is still controversial. Therefore, the role of NO production in the pathogenesis of hypoxic pulmonary hypertension remained to be elucidated. METHODS: We measured the NOx production during acute and chronic hypoxia in anesthetized rats and determined effects of NOS inhibitor in the hemodynamic responses to hypoxic exposure. Catheterization of the pulmonary artery, femoral artery, and femoral vein were done for monitoring the arterial pressure and for drug administration. The cardiac output was determined by using Cardiomax II (Columbus Inc., OHIO). RESULTS: The total systemic vascular resistance reduced by 41+/-11percent, whereas the pulmonary vascular resistance increased by 25+/-12percent during acute hypoxia. Pretreatment with L-NAME (25 mg/kg) attenuated the systemic vasodilatation and enhanced the pulmonary vasoconstriction. In rats prior exposure to hypobaric (0.5 ATA) hypoxia for 15 days (CH-15 group), the baseline mean pulmonary and systemic arterial pressures were significantly higher than those in the control group (42+/-5 vs. 29+/-3 mmHg and 102+/-5 vs. 88+/-11 mmHg, respectively). Chronic hypoxia also caused a right ventricular hypertrophy as evidenced by a greater RV/LV+S ratio compared to the control group (46+/-4percent vs. 28+/-3percent). In the CH-15 group, acute hypoxia elicited a decrease in systemic vascular resistance by 14+/-13percent. Conclusion: Our results suggested that acute hypoxia may elicit pulmonary vasoconstriction via an unknown pathway, causing passive release of nitric oxide for counteracting the pulmonary vasoconstriction, but resulting in profoundly systemic vasodilatation. These hemodynamic responses were attenuated after a sustained exposure to chronic hypoxia.
Description: Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org )
URI: http://archive.rubicon-foundation.org/993
Date: 2001

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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