Sobey C G, Heistad D D, Faraci F M
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242-1081, USA.
Stroke. 1997 Feb;28(2):392-6; discussion 396-7. doi: 10.1161/01.str.28.2.392.
Cerebral vasodilatation in response to aprikalim, an opener of ATP-sensitive K+ channels, is selectively augmented after subarachnoid hemorrhage (SAH). Vasodilatation in response to activation of ATP-sensitive K+ channels, however, is impaired during chronic hypertension. Hypertension may contribute to a worse outcome after SAH, but the nature of the relationship between hypertension and SAH is uncertain. In the present study we examined responses of the basilar artery to aprikalim after SAH in normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP).
In anesthetized WKY and SHRSP, we measured changes in diameter of the basilar artery in response to aprikalim and papaverine using a cranial window 2 days after injection of 0.3 mL saline or autologous blood into the cistema magna.
Under control conditions, aprikalim (0.1 to 1 mumol/L) and papaverine (10 to 100 mumol/L) produced dilatation of the basilar artery. After SAH, responses to aprikalim were not significantly altered in WKY and were markedly increased in SHRSP compared with saline-injected control rats. In contrast, vasodilator responses to papaverine were not changed by SAH in either WKY or SHRSP, suggesting that augmented vasodilatation in response to aprikalim after SAH was selective.
Responses of the basilar artery to aprikalim were greatly augmented in SHRSP after SAH. Because vasodilator responses to many stimuli are impaired after SAH and cerebral vasodilator responses to several stimuli are impaired by chronic hypertension, augmented responses to activation of K+ channels despite the presence of hypertension are unusual.
ATP敏感性钾通道开放剂阿普卡林引起的脑血管扩张在蛛网膜下腔出血（SAH）后选择性增强。然而，在慢性高血压期间，ATP敏感性钾通道激活引起的血管扩张受损。高血压可能导致SAH后预后更差，但高血压与SAH之间关系的本质尚不确定。在本研究中，我们检测了正常血压的Wistar-Kyoto大鼠（WKY）和易中风自发性高血压大鼠（SHRSP）在SAH后基底动脉对阿普卡林的反应。
在麻醉的WKY和SHRSP中，于向大池内注射0.3 mL生理盐水或自体血2天后，使用颅窗测量基底动脉直径对阿普卡林和罂粟碱的变化。
在对照条件下，阿普卡林（0.1至1 μmol/L）和罂粟碱（10至100 μmol/L）可使基底动脉扩张。SAH后，与注射生理盐水的对照大鼠相比，WKY对阿普卡林的反应无明显改变，而SHRSP的反应显著增加。相比之下，WKY和SHRSP中SAH均未改变对罂粟碱的血管舒张反应，这表明SAH后对阿普卡林的血管扩张增强具有选择性。
SAH后SHRSP基底动脉对阿普卡林的反应大幅增强。由于SAH后对多种刺激的血管舒张反应受损，且慢性高血压会损害脑血管对多种刺激的舒张反应，因此尽管存在高血压，对钾通道激活的反应增强仍不常见。
