Impaired endothelium-dependent relaxation in rabbit pulmonary artery after subarachnoid hemorrhage.
Impaired endothelium-dependent relaxation in rabbit pulmonary artery after subarachnoid hemorrhage.
复制标题
蛛网膜下腔出血后兔肺动脉内皮依赖性舒张受损。
DOI：
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发表时间：
1996
影响因子：
3
通讯作者：
K. Hirakawa
中科院分区：
文献类型：
--
作者：
E. Isotani;H. Azuma;R. Suzuki;H. Hamasaki;J. Sato;K. Hirakawa
本文观察了兔脑池注血致蛛网膜下腔出血（SAH）后肺动脉和基底动脉内皮功能的变化。在第2天和第7天处死动物，并在主肺动脉的横向条和从基底动脉采集的环上测定机械反应。为了检查迷走神经的作用，我们在注射脑池血液之前立即切断左侧迷走神经。去内皮后，肺动脉和基底动脉对乙酰胆碱（ACh）和A23187的舒张反应被消除，而对乙酰胆碱和A23187的舒张反应被N-硝基-L-精氨酸（NOARG）或亚甲蓝（MB）抑制。吲哚美辛未能改变这些松弛反应。12只家兔中有6只在第2天肺动脉条对ACh的舒张反应明显减弱（p < 0.05和p < 0.01）。在其余6只家兔中，舒张未受影响。对A23187和硝普钠（SNP）的舒张反应在任何12例中均未观察到变化。在迷走神经切断的家兔中，未观察到对ACh的反应降低。第7天，ACh舒张反应恢复正常。乙酰胆碱也产生了减少舒张基底动脉环在第2天没有变化，A23187和SNP诱导的舒张。SAH后肺动脉和基底动脉对去甲肾上腺素（NE）、内皮素-1（ET-1）、5-羟色胺（5-HT）和U46619的收缩反应不受影响。这些结果表明，功能较低的毒蕈碱受体，产生/释放较少的内皮源性舒张因子[EDRF/一氧化氮（NO）]参与引起SAH后肺动脉和基底动脉的舒张减少，迷走神经可能在调节受体介导的内皮依赖性舒张中发挥作用。
We investigated the changes in endothelial function of pulmonary as well as basilar artery after experimental subarachnoid hemorrhage (SAH) induced by cisternal blood injection in rabbits. The animals were killed on day 2 and day 7, and the mechanical responses were determined on transverse strips of the main pulmonary artery and rings harvested from the basilar artery. To examine the role of the vagal nerve, we cut the left vagal nerve immediately before injecting cisternal blood. Relaxation response of pulmonary and basilar arteries to acetylcholine (ACh) and A23187 were abolished after endothelial removal and reality inhibited by either NG-nitro-L-arginine (NOARG) or methylene blue (MB). Indomethacin failed to modify these relaxation responses. Relaxation response of the main pulmonary artery strips to ACh was significantly (p < 0.05 and p < 0.01) attenuated on day 2 in 6 of 12 rabbits. In the remaining 6 rabbits, relaxation was not affected. No change in relaxation responses to A23187 and sodium nitroprusside (SNP) was observed in any of the 12 cases. In the vagotomized rabbits no decreased response to ACh was observed. On day 7, relaxation response to ACh returned to normal. ACh also produced decreased relaxation in basilar artery rings on day 2 with no change in A23187- and SNP-induced relaxation. Contractile responses of pulmonary and basilar arteries to norepinephrine (NE), endothelin-1 (ET-1), 5-hydroxytryptamine (5-HT), and U46619 were not affected after SAH. These results suggest that less functional muscarinic receptors that produce/release less endothelium-derived relaxation factor [EDRF/nitric oxide (NO)] are involved in causing the reduced relaxation of pulmonary and basilar arteries after SAH and the vagal nerve may play a role in regulating the receptor-mediated, endothelium-dependent relaxation in the main pulmonary artery after experimental SAH.
血管平滑肌中硝普钠代谢激活一氧化氮。
DOI：
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发表时间：
1992
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Kowaluk,EA;Seth,P;Fung,HL
通讯作者：
Fung,HL