Macro-and Micropulmonary Hemodynamic Changes to Nitric Oxide Blockade in Monocrotaline-Induced Pulmonary Hypertension IN Rats-An in Vivo Approach

一氧化氮阻斷對monocrotaline造成之大鼠肺動脈高血壓的影響：活體肺循環與肺微循環之探討

陳昌文(Chang-Wen Chen) ； 王景明(Ching-Min Wang) ； 李政宏(Cheng-Hung Lee) ； 薛尊仁(Tzuen-Ren Hsiue) ； 郭育良(Yu-Liang Kuo) ； 張漢煜(Han-Yu Chang)

《Journal of the Formosan Medical Association》 104卷5期 (2005/05) Pp. 301-307

https://doi.org/10.29828/JFMA.200505.0001

並列摘要

Background and Purpose: Data on the role of nitric oxide (NO) in monocrotaline (MC)-induced pulmonary hypertension of rats have all been derived from in vitro measurements. In vivo pulmonary hypertension and microvascular responses to NO blockade in MC-treated rats have not been reported. The current study evaluated
the role of NO in live MC-treated rats.
Methods: Male Sprague-Dawley rats (n=29) were divided into saline control and MC-treated groups. Three to 4 weeks after either saline or MC injection, pulmonary hemodynamics were measured using pulmonary arterial catheter and thermodilution techniques. Pulmonary microvascular diameter changes were assessed using an intravital microscope.
Results: Three to 4 weeks after subcutaneous injection of MC (50 mg/kg), MC-treated rats showed elevated pulmonary arterial pressure compared to control rats (23.6±2.9mm Hg vs 14.5±0.8mm Hg). N(superscript ω)-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg, intravenously), an NO synthase inhibitor, produced significant increases in pulmonary arterial pressure and total pulmonary vascular resistance compared to control rats (12.3±2.5mm Hg vs 1.0±0.9mm Hg; 0.21±0.04 mm Hg/mL/min vs 0.05±0.02mm Hg/mL/min, p＜0.05). Intravital microscopic observation of the subpleural vessels showed significant vasoconstriction in medium-sized (＞40 μm) pulmonary arterioles of MC-treated rats following L-NAIVW administration (58.4±3.6μm vs 47.1±3.4μm, p＜0.05) while no significant diameter changes were found in either the small-sized (＜40μm) pulmonary arterioles or pulmonary venules. Diameters of pulmonary arterioles and venules in control rats were not affected by L-NAME administration.
Conclusion: Pulmonary arterial pressure and pulmonary vascular resistance increased after NO blockade in live MC-treated rats. The site of vasoconstriction after NO blockade included medium-sized pulmonary arterioles but not small-sized pulmonary arterioles. This study has provided both macro-and microhemodynamic evidence of a modulatory role of NO in live MC-treated rats.

並列關鍵字

Enzyme inhibitors ； Microcirculation ； Monocrotaline ； Nitric oxide ； Pulmonary hypertension