Donahue D M, Lee M E, Suen H C, Quertermous T, Wain J C
Department of Surgery, Harvard Medical School, Boston, Massachusetts.
J Surg Res. 1994 Aug;57(2):280-3. doi: 10.1006/jsre.1994.1145.
The hypoxic pulmonary vasoconstrictor response (HPVR) is a physiologic mechanism for directing pulmonary blood flow to nonhypoxic regions of the lung. The mechanism of this response remains unclear. To investigate the role of endothelin-1 (ET-1), a potent vasoconstrictor produced by vascular endothelium, in HPVR an in vivo model of alveolar hypoxia was developed. When one lung in an anesthetized sheep was made hypoxic, the static ET-1 mRNA levels in lung tissue increased in proportion to the observed decrease in pulmonary blood flow (Qp) to that lung. With reversal of hypoxia, Qp and ET-1 levels returned to baseline. This relationship between alveolar hypoxia and ET-1 mRNA levels suggests a role for ET-1 in the local pulmonary response to hypoxia.
缺氧性肺血管收缩反应（HPVR）是一种将肺血流导向肺非缺氧区域的生理机制。这种反应的机制尚不清楚。为了研究血管内皮产生的强效血管收缩剂内皮素-1（ET-1）在HPVR中的作用，建立了一种肺泡缺氧的体内模型。当麻醉绵羊的一侧肺缺氧时，肺组织中静态ET-1 mRNA水平与该侧肺观察到的肺血流量（Qp）下降成比例增加。随着缺氧的逆转，Qp和ET-1水平恢复到基线。肺泡缺氧与ET-1 mRNA水平之间的这种关系表明ET-1在局部肺对缺氧的反应中起作用。
