Maintained endothelium-dependent pulmonary vasodilation following chronic hypoxia in the rat.
Maintained endothelium-dependent pulmonary vasodilation following chronic hypoxia in the rat.
复制标题
大鼠慢性缺氧后维持内皮依赖性肺血管舒张。
DOI：
10.1152/jappl.1993.74.1.339
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Walker,BR
中科院分区：
文献类型：
--
作者：
Russ,RD;Walker,BR
我们以前已经证明，精氨酸加压素（AVP）通过释放一氧化氮（NO）扩张预收缩的肺血管。然而，最近的证据表明，在长期暴露于缺氧的动物的肺中，响应于其他药剂的NO释放可能受到抑制。本实验的目的是确定加压素能肺血管舒张是否受到慢性缺氧（大气压= 380托，持续4周）的类似影响。用N ω-硝基-L-精氨酸（L-NNA）抑制NO合成对对照组或慢性缺氧大鼠离体盐灌注肺的基线灌注压没有影响。同样，肺血管舒张反应AVP和钙离子载体A23187不受慢性缺氧暴露。预处理与环氧合酶抑制剂meclutamate没有改变肺血管加压素能肺血管舒张，无论是控制或慢性缺氧动物，排除参与血管扩张剂arylandins在响应AVP。与此相反，AVP和A23187的血管舒张反应抑制L-NNA预处理不仅在对照动物的肺，但也在肺慢性缺氧大鼠，表明NO参与的血管舒张反应。L-NNA的抑制作用可通过预先加入过量的L-精氨酸而不是D-精氨酸来逆转。此外，血管舒张反应的内皮非依赖性血管扩张剂硝普钠和异丙肾上腺素的慢性缺氧暴露的影响。我们的结论是，内皮依赖性血管舒张在雄性SD大鼠慢性缺氧暴露后保持完整。
We have previously demonstrated that arginine vasopressin (AVP) dilates the preconstricted pulmonary vasculature via the release of nitric oxide (NO). However, recent evidence suggests that NO release in response to other agents may be suppressed in lungs from animals that have been chronically exposed to hypoxia. The purpose of the present experiment was to determine whether vasopressinergic pulmonary vasodilation is similarly affected by chronic exposure to hypoxia (barometric pressure = 380 Torr for 4 wk). Inhibition of NO synthesis with N omega-nitro-L-arginine (L-NNA) had no effect on baseline perfusion pressure in isolated salt-perfused lungs from either control or chronically hypoxic rats. Similarly, pulmonary vasodilatory responses to AVP and the calcium ionophore A23187 were unaffected by chronic hypoxic exposure. Pretreatment with the cyclooxygenase inhibitor meclofenamate did not alter vasopressinergic pulmonary vasodilation in lungs from either control or chronically hypoxic animals, ruling out involvement of vasodilator prostaglandins in the response to AVP. In contrast, vasodilatory responses to both AVP and A23187 were inhibited by L-NNA pretreatment not only in lungs from control animals but also in lungs from chronically hypoxic rats, suggesting the involvement of NO in the vasodilatory response. The inhibition by L-NNA was reversible by prior addition of excess L-arginine but not by D-arginine. In addition, vasodilatory responses to the endothelium-independent vasodilators sodium nitroprusside and isoproterenol were unaffected by chronic hypoxic exposure. We conclude that endothelium-dependent vasodilation remains intact in male Sprague-Dawley rats after chronic hypoxic exposure.