RESPONSES OF CEREBRAL-ARTERIES AFTER ISCHEMIA AND REPERFUSION IN CATS
RESPONSES OF CEREBRAL-ARTERIES AFTER ISCHEMIA AND REPERFUSION IN CATS
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DOI：
10.1152/ajpheart.1988.255.4.h879
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发表时间：
1988-10-01
影响因子：
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通讯作者：
HEISTAD, DD
中科院分区：
文献类型：
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作者：
MAYHAN, WG;AMUNDSEN, SM;HEISTAD, DD
我们的目的是确定脑缺血和再灌注后脑动脉的反应是否改变。测量脑动脉直径（150-180 .mu）。m)猫对局部应用乙酰胆碱（ACh）和血清素的反应，它们会释放内皮源性松弛因子（EDRF），而腺苷和血管紧张素则不会释放EDRF。当基线直径恢复到控制水平时，在脑缺血10或30分钟前后测量动脉直径。在对照条件下，血清素和血管紧张素使脑动脉收缩16.5%。2和23，+-。3%（平均值+-）。乙酰胆碱和腺苷分别使脑动脉扩张22。2和23，+-。3%,分别。脑缺血10 min再灌注时，脑动脉收缩反应得以保留。缺血10分钟后，动脉对乙酰胆碱的血管扩张反应是不均匀的。在6 - 15只猫中，乙酰胆碱引起的血管扩张得以保留。相比之下，在15只猫中，有9只猫对乙酰胆碱反应的血管舒张功能受损(7。3%)。在缺血10分钟后，两组对腺苷的血管舒张反应均未受损。脑缺血30min再灌注时，脑动脉收缩反应得以保留。相反，脑动脉扩张对乙酰胆碱和腺苷的反应受到损害。我们推测缺血后脑血管舒张受损，血管收缩维持，可能导致脑缺血后再灌注受损。
Our goal was to determine whether responses of cerebral arteries are altered after cerebral ischemia and reperfusion. We measured diameter of cerebral arteries (150-180 .mu.m) in cats in response to topical application of acetylcholine (ACh) and serotonin, which release endothelium-derived relaxing factor (EDRF), and adenosine and angiotensin, which do not release EDRF. Diameter of arteries was measured before and after 10 or 30 min of cerebral ischemia, when base-line diameter had returned to control levels. Under control conditions, serotonin and angiotensin constricted cerebral arteries by 16 .+-. 2 and 23 .+-. 3% (means .+-. SE), respectively, and ACh and adenosine dilated cerebral arteries by 22 .+-. 2 and 23 .+-. 3%, respectively. During reperfusion after 10 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. Vasodilator responses of arteries to ACh after 10 min of ischemia were heterogeneous. In 6 to 15 cats, vasodilatation in reponse to ACh was preserved. In contrast, in 9 of 15 cats, vasodilatation in response to ACh was impaired (7 .+-. 3%). In both groups, vasodilatation in response to adenosine was not impaired after 10 min of ischemia. During reperfusion after 30 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. In contrast, dilatation of cerebral arteries in response to ACh and adenosine was impaired. We speculate that impaired cerebral vasodilatation after ischemia, with maintenance of vasoconstriction, may contribute to impaired reperfusion after cerebral ischemia.