Yao H, Sadoshima S, Shiokawa O, Fujii K, Fujishima M
Stroke. 1987 May-Jun;18(3):629-33. doi: 10.1161/01.str.18.3.629.
The influences of acute cerebral ischemia on renal hemodynamics were examined in spontaneously hypertensive rats in which cerebral ischemia was induced by bilateral carotid artery occlusion. Renal and cerebral blood flow were measured with a hydrogen clearance technique. Either phenoxybenzamine (0.5 mg/kg body wt) or propranolol (2 mg/kg) was given i.v. immediately after ischemia was induced to examine the drugs' effects on cerebral and renal hemodynamics. One hour after ischemia, cerebral blood flow was markedly reduced to 5, 3, and almost 0% of the preischemic value in the untreated, phenoxybenzamine-treated, and propranolol-treated rats, respectively. In contrast, renal blood flow at that time was decreased to 65, 88, and 67%, respectively. The calculated renal vascular resistance was similarly increased to 151% in the untreated and 136% in the propranolol-treated rats, but decreased to 82% in the phenoxybenzamine-treated rats. The present results indicate that in acute cerebral ischemia renal blood flow was considerably decreased with concomitant increased renal vascular resistance, and that such reduction in renal blood flow was minimized by alpha-adrenergic blockade but not by beta-blockade. It is concluded that activation of the alpha-adrenergic system in acute cerebral ischemia causes renal vasoconstriction.
在自发性高血压大鼠中，通过双侧颈动脉闭塞诱导脑缺血，研究急性脑缺血对肾血流动力学的影响。用氢清除技术测量肾和脑血流量。在诱导缺血后立即静脉注射苯氧苄胺（0.5mg/kg体重）或普萘洛尔（2mg/kg），以检查药物对脑和肾血流动力学的影响。缺血1小时后，未治疗组、苯氧苄胺治疗组和普萘洛尔治疗组的脑血流量分别显著降低至缺血前值的5%、3%和几乎0%。相比之下，此时肾血流量分别降至65%、88%和67%。计算得出的肾血管阻力在未治疗组中同样增加至151%，在普萘洛尔治疗组中增加至136%，但在苯氧苄胺治疗组中降至82%。目前的结果表明，在急性脑缺血时，肾血流量显著减少，同时肾血管阻力增加，并且这种肾血流量的减少通过α-肾上腺素能阻滞而不是β-阻滞剂最小化。得出的结论是，急性脑缺血时α-肾上腺素能系统的激活导致肾血管收缩。
