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首页> 外文期刊>American Journal of Physiology >Inhaled nitric oxide-induced rebound pulmonary hypertension: role for endothelin-1.
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Inhaled nitric oxide-induced rebound pulmonary hypertension: role for endothelin-1.

机译：吸入一氧化氮诱导的反弹性肺动脉高压：内皮素-1的作用。

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摘要

Clinically significant increases in pulmonary vascular resistance have been noted on acute withdrawal of inhaled nitric oxide (NO). Endothelin (ET)-1 is a vasoactive peptide produced by the vascular endothelium that may participate in the pathophysiology of pulmonary hypertension. The objectives of this study were to determine the effects of inhaled NO on endogenous ET-1 production in vivo in the intact lamb and to determine the potential role of ET-1 in the rebound pulmonary hypertension associated with the withdrawal of inhaled NO. Seven 1-mo-old vehicle-treated control lambs and six PD-156707 (an ET(A) receptor antagonist)-treated lambs were mechanically ventilated. Inhaled NO (40 parts per million) was administered for 24 h and then acutely withdrawn. After 24 h of inhaled NO, plasma ET-1 levels increased by 119.5 +/- 42.2% (P < 0.05). Western blot analysis revealed that protein levels of preproET-1, endothelin-converting enzyme-1alpha, and ET(A) and ET(B) receptors were unchanged. On acute withdrawal of NO, pulmonary vascular resistance (PVR) increased by 77.8% (P < 0.05) in control lambs but was unchanged (-5.5%) in PD-156707-treated lambs. Inhaled NO increased plasma ET-1 concentrations but not gene expression in the intact lamb, and ET(A) receptor blockade prevented the increase in PVR after NO withdrawal. These data suggest a role for ET-1 in the rebound pulmonary hypertension noted on acute withdrawal of inhaled NO.
机译：吸入一氧化氮（NO）急性停药时，肺血管阻力的临床显着增加已被注意到。内皮素（ET）-1是由血管内皮产生的血管活性肽，可能参与肺动脉高压的病理生理。这项研究的目的是确定吸入的NO对完整羔羊体内内源性ET-1产生的影响，并确定ET-1在与吸入NO撤出相关的反弹性肺动脉高压中的潜在作用。对7只1个月大的用媒介物处理过的对照羔羊和6只PD-156707（一种ET（A）受体拮抗剂）处理过的羔羊进行机械通风。吸入NO（百万分之40）进行24小时给药，然后迅速撤出。吸入NO 24小时后，血浆ET-1水平增加了119.5 +/- 42.2％（P <0.05）。蛋白质印迹分析表明，preproET-1，内皮素转化酶-1α，ET（A）和ET（B）受体的蛋白水平没有变化。急性撤离NO后，对照羔羊的肺血管阻力（PVR）增加了77.8％（P <0.05），但PD-156707处理过的羔羊的肺血管阻力没有改变（-5.5％）。吸入NO会增加血浆ET-1的浓度，但不会影响完整羔羊的基因表达，而ET（A）受体阻滞阻止NO撤出后PVR的增加。这些数据表明，ET-1在吸入NO急性停药时出现的反弹性肺动脉高压中起作用。

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