Bradykinin-induced increase in pulmonary vascular permeability in hypoxic sheep.
Bradykinin-induced increase in pulmonary vascular permeability in hypoxic sheep.
复制标题
缓激肽诱导缺氧羊肺血管通透性增加。
DOI：
10.1152/jappl.1982.52.2.370
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Stalcup,SA
中科院分区：
文献类型：
--
作者：
Pang,LM;O'Brodovich,HM;Mellins,RB;Stalcup,SA
缓激肽（BK）是一种强有力的全身组织水肿剂。它被血管紧张素转换酶（ACE）降解，ACE位于所有血管内皮细胞的表面。我们假设，由于氧分压调节ACE活性，高肺氧分压，因此高ACE活性保护肺从BK的致水肿作用。因此，我们研究了外源性BK在未麻醉绵羊手术创建的淋巴瘘和血管导管在常氧和缺氧的影响。BK显着升高肺淋巴流量和蛋白质流量只有当绵羊缺氧和肺的能力，降解BK受损。这种增加不能归因于血管表面积的募集或液体交换驱动力的增加，因为肺动脉或左心房压力、心输出量或肺血管阻力没有变化。我们得出结论，BK通过增加血管通透性增加肺中的水和蛋白质运动。
Bradykinin (BK) is a potent edematogenic agent in systemic tissues. It is degraded by angiotensin-converting enzyme (ACE), which is located on the surface of all vascular endothelia. We hypothesized that since oxygen tension modulates ACE activity, the high pulmonary oxygen tension and hence high ACE activity protects the lung from the edematogenic effects of BK. We therefore studied the effect of exogenous BK in unanesthetized sheep with surgically created lymph fistulas and vascular catheters during normoxia and hypoxia. BK significantly elevated lung lymph flow and protein flux only when the sheep were made hypoxic and the lung's ability to degrade BK was impaired. This increase could not be attributed to recruitment of vascular surface area or to an increase in the driving force for fluid exchange because there were no changes in pulmonary arterial or left atrial pressures, cardiac output, or pulmonary vascular resistance. We conclude that BK increases water and protein movement in the lung by increasing vascular permeability.