Akiguchi I, Horie R, Yamori Y
Stroke. 1980 Jul-Aug;11(4):383-9. doi: 10.1161/01.str.11.4.383.
Dopamine and norepinephrine fluorescence in the nucleus caudatus and putamen and cerebral cortex was markedly depleted along with rCBF reduction in symptomatic stroke-prone spontaneously hypertensive rats (SHRSP) with bilateral carotid artery ligation under light pentobarbital anesthesia. An accumulation of fluorescence at the intima of blood vessels, especially in the nucleus caudatus and putamen, was noted in some SHRSP under the same experimental conditions. These changes were hardly seen in deeply anesthetized SHRSP, as well as in normotensive Wistar-Kyoto (WK) rats. It may be possible, therefore, that released cerebral amines in acute brain ischemia accelerate the vasoconstriction and permeability of cerebral arteries, which further decreases the blood supply to these areas. Also, a barbiturate protective effect against the release of central dopamine and norepinephrine during acute brain ischemia was noted in deeply anesthetized SHRSP.
在轻度戊巴比妥麻醉下双侧颈总动脉结扎的有症状的易中风自发性高血压大鼠(SHRSP)中,尾状核、壳核和大脑皮质中的多巴胺和去甲肾上腺素荧光随着局部脑血流量(rCBF)的减少而明显耗竭。在相同实验条件下,一些SHRSP的血管内膜,尤其是尾状核和壳核处出现荧光积聚。在深度麻醉的SHRSP以及正常血压的Wistar-Kyoto(WK)大鼠中几乎未见这些变化。因此,急性脑缺血时释放的脑胺可能会加速脑动脉的血管收缩和通透性,进而减少这些区域的血液供应。此外,在深度麻醉的SHRSP中还观察到巴比妥类药物对急性脑缺血期间中枢多巴胺和去甲肾上腺素释放的保护作用。