Responses to vasodilator drugs on pulmonary artery preparations from pulmonary hypertensive rats
Responses to vasodilator drugs on pulmonary artery preparations from pulmonary hypertensive rats
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肺动脉高压大鼠肺动脉制剂对血管扩张药物的反应
DOI：
10.1111/j.1476-5381.1992.tb14227.x
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发表时间：
1992
影响因子：
7.3
通讯作者：
S. O'donnell
中科院分区：
文献类型：
--
作者：
J. Wanstall;S. O'donnell
1 使用取自野百合碱或慢性缺氧引起的肺动脉高压的大鼠的肺动脉和主动脉去甲肾上腺素 (0.1 μm) 收缩环制剂，检查了六种具有不同作用机制的血管扩张药物的松弛反应。 2 在野百合碱治疗大鼠的肺动脉制剂中，与对照组相比，(a) 吡那地尔和克罗卡林的最大舒张值显着增加，但其效力（负 log EC50）没有变化，(b) 硝普钠和亚硝酸钠的效力显着降低（分别为 10 倍和 3 倍），但最大值没有变化，(c) 尼可地尔的最大松弛度增加，而效力降低（3倍），并且（d）对于心肽II，效力或最大值没有变化。 3 在患有慢性缺氧性肺动脉高压的大鼠的肺动脉制剂中也证明了吡那地尔最大松弛度的增加和硝普钠效力的降低。其他四种药物未在缺氧大鼠的制剂中进行检查。 4 在两种肺动脉高压模型中，主动脉制剂对任何血管扩张药物的最大反应或效力均未见变化。 5 在对照制剂中，没有一种药物对肺动脉的作用比对主动脉的作用更强（即它们不是肺选择性的）。在肺动脉高压大鼠的制剂中，吡那地尔对肺动脉具有选择性，而硝普钠对主动脉具有选择性。 6 结论是，大鼠肺动脉高压的发生伴随着肺动脉对某些血管扩张药物的反应性的变化；这些变化是否发生取决于血管扩张药物的作用机制；但它们与诱发肺动脉高压的方法无关。 7 据推测，硝普钠、亚硝酸钠和尼可地尔的效力降低可能是由于肺动脉高压时肺血管平滑肌中可溶性鸟苷酸环化酶的脱敏所致。
1 Relaxant responses to six vasodilator drugs, with different mechanisms of action, were examined on noradrenaline (0.1 μm)‐contracted ring preparations of pulmonary artery and aorta taken from rats with pulmonary hypertension induced by monocrotaline or chronic hypoxia. 2 On pulmonary artery preparations from monocrotaline‐treated rats, compared with controls, (a) the maximum relaxation to pinacidil and cromakalim was significantly increased, but their potency (negative log EC50) was unchanged, (b) the potencies of nitroprusside and sodium nitrite were significantly reduced (10 fold and 3 fold respectively), but there was no change in the maxima, (c) for nicorandil there was an increase in maximum relaxation and a decrease in potency (3 fold), and (d) for atriopeptin II there was no change in potency or maximum. 3 The increase in maximum relaxation for pinacidil and the decrease in potency for nitroprusside were also demonstrated in pulmonary artery preparations from rats with chronic hypoxic pulmonary hypertension. The other four drugs were not examined in preparations from hypoxic rats. 4 In both models of pulmonary hypertension, no change in maximum response or potency was seen on aortic preparations for any of the vasodilator drugs. 5 In control preparations, none of the drugs was more potent on pulmonary artery than on aorta (i.e. they were not pulmonary‐selective). In preparations from pulmonary hypertensive rats, pinacidil was selective for pulmonary artery, in contrast to nitroprusside which was selective for aorta. 6 It is concluded that the development of pulmonary hypertension in rats is accompanied by changes in the responsiveness of the pulmonary arteries to some vasodilator drugs; whether or not these changes occur depends on the mechanism of action of the vasodilator drug; but they are independent of the method of inducing pulmonary hypertension. 7 It is postulated that the reduction in potency seen for nitroprusside, sodium nitrite and nicorandil may be due to desensitization of soluble guanylate cyclase in pulmonary vascular smooth muscle in pulmonary hypertension.
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野百合碱吡咯诱导的肺动脉高压大鼠肺部血管反应性增加。
DOI：
10.1164/arrd.1985.131.1.46
发表时间：
1985
期刊：
The American review of respiratory disease
影响因子：
--
作者：
Hilliker,KS;Roth,RA
通讯作者：
Roth,RA
DOI：
10.1164/arrd.1986.134.2.342
发表时间：
1986-08
期刊：
The American review of respiratory disease
影响因子：
--
作者：
J. Reeves;B. Groves;D. Turkevich
通讯作者：
J. Reeves;B. Groves;D. Turkevich
影响因子：
15.9
作者：
BRASHERS, VL;PEACH, MJ;ROSE, CE
通讯作者：
ROSE, CE
影响因子：
56.9
作者：
STANDEN, NB;QUAYLE, JM;NELSON, MT
通讯作者：
NELSON, MT