ENHANCED PULMONARY ARTERIAL DILATION TO ARGININE-VASOPRESSIN IN CHRONICALLY HYPOXIC RATS
ENHANCED PULMONARY ARTERIAL DILATION TO ARGININE-VASOPRESSIN IN CHRONICALLY HYPOXIC RATS
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DOI：
10.1152/ajpheart.1994.267.6.h2413
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发表时间：
1994-12-01
影响因子：
4.8
通讯作者：
WALKER, BR
中科院分区：
文献类型：
--
作者：
EICHINGER, MR;WALKER, BR
慢性低氧暴露诱发肺血管重构，并可能改变正常的肺内皮功能。我们研究了血管舒张反应的受体介导的内皮依赖性扩张剂精氨酸加压素（AVP），非受体介导的内皮依赖性扩张剂A-23187，和一氧化氮（NO）供体硝普钠从控制或慢性缺氧大鼠肺分离。从雄性Sprague-Dawley大鼠中分离肺，并用含有4%白蛋白的生理盐水溶液灌注。监测动脉和静脉压力，通过双闭塞估计微血管压力，以评估节段性阻力。平衡后，用血栓烷模拟物U-46619使肺收缩。当出现稳定的按压反应时，用上述药物之一扩张肺部。将一系列剂量的AVP施用到与对照组或慢性缺氧大鼠不同的肺组。与对照组相比，慢性缺氧大鼠肺对AVP的舒张反应增强，这种效应是由于毛细血管前段的扩张增强所致。两组肺对A-23187和硝普钠的总体和节段性血管舒张反应无差异，提示慢性缺氧并不上调NO合酶或增强血管平滑肌对NO的反应性。因此，我们的数据提示慢性缺氧后AVP增强的总动脉和肺动脉扩张最有可能是由于受体-调节激素的过程。
Chronic hypoxic exposure elicits pulmonary vascular remodeling and may alter normal pulmonary endothelial function. We examined the vasodilatory response to the receptor-mediated endothelium-dependent dilator arginine vasopressin (AVP), the nonreceptor-mediated endothelium-dependent dilator A-23187, and the nitric oxide (NO) donor sodium nitroprusside in lungs isolated from control or chronically hypoxic rats. Lungs were isolated from male Sprague-Dawley rats and perfused with a physiological saline solution containing 4% albumin. Arterial and venous pressures were monitored and microvascular pressure was estimated by double occlusion, allowing assessment of segmental resistances. After equilibration, lungs were constricted with the thromboxane mimetic U-46619. Upon development of a stable presser response, lungs were dilated with one of the above agents. A series of doses of AVP was administered to separate groups of lungs from control or chronically hypoxic rats. Lungs from chronically hypoxic rats exhibited an augmented dilatory response to AVP compared with control lungs, and this effect was due to enhanced dilation of precapillary segments. The total and segmental vasodilatory responses to A-23187 and sodium nitroprusside were not different between the two groups of lungs, suggesting that chronic hypoxia did not upregulate the enzyme NO synthase or enhance the vascular smooth muscle responsiveness to NO. Thus our data suggest that the augmented total and pulmonary arterial dilation to AVP after chronic hypoxia is most likely due to altered receptor-mediated processes of the hormone.