Irikura K, Morii S, Miyasaka Y, Yamada M, Tokiwa K, Yada K
Department of Neurosurgery, Kitasato University School of Medicine, Kanagawa, Japan.
Stroke. 1996 Aug;27(8):1399-404. doi: 10.1161/01.str.27.8.1399.
To verify the hypothesis that impaired autoregulation may contribute to cerebral swelling or hemorrhage after a sudden recovery of perfusion pressure, we studied the chronic effects of cerebral hypoperfusion on the autoregulatory responses of the pial arterioles in situ.
Eight to 12 weeks after a carotid-jugular fistula was created in rats, experiments were performed under alpha-chloralose and urethane anesthesia. Regional cerebral blood flow (rCBF) was determined by the hydrogen clearance method, and carotid pressure was measured. Using a closed cranial window, we determined the autoregulatory responses of the arterioles (30 to 50 microns) to both hypertension induced by norepinephrine and sudden fistula closure at various mean arterial pressures (MAPs).
rCBF on the fistula side was reduced by 27%. Carotid pressure was significantly lower than normal but was immediately increased by fistula closure. The pial arterioles showed marked elongation and enlargement. During induced hypertension, the arterioles in the fistula group started to dilate at an MAP lower than that of the control group (130 versus 180 mm Hg, respectively). The arterioles constricted when the fistula was occluded at normal MAP. However, when the fistula was occluded at an MAP higher than 130 mm Hg, the vessels dilated.
It was demonstrated that (1) chronic hypoperfusion induced impairment of the upper limit of autoregulation and (2) sudden fistula closure under hypertensive conditions caused vasodilation of the arterioles. These findings suggest that rapid restoration of perfusion pressure is possibly followed by a pressure breakthrough phenomenon in a chronically hypoperfused cerebrovasculature.
为验证灌注压突然恢复后自动调节功能受损可能导致脑肿胀或出血这一假说，我们研究了脑灌注不足对在位软脑膜小动脉自动调节反应的慢性影响。
在大鼠建立颈静脉瘘8至12周后，于α-氯醛糖和乌拉坦麻醉下进行实验。采用氢清除法测定局部脑血流量（rCBF），并测量颈动脉压力。通过闭合的颅骨视窗，我们测定了小动脉（30至50微米）在不同平均动脉压（MAP）下对去甲肾上腺素诱导的高血压以及瘘管突然闭合的自动调节反应。
瘘管侧的rCBF降低了27%。颈动脉压力显著低于正常水平，但瘘管闭合后立即升高。软脑膜小动脉显示出明显的伸长和扩张。在诱导高血压期间，瘘管组的小动脉在低于对照组的MAP时开始扩张（分别为130毫米汞柱和180毫米汞柱）。当在正常MAP下闭塞瘘管时，小动脉收缩。然而，当在高于130毫米汞柱的MAP下闭塞瘘管时，血管扩张。
结果表明，（1）慢性灌注不足导致自动调节上限受损，（2）高血压条件下瘘管突然闭合导致小动脉扩张。这些发现提示，在长期灌注不足的脑血管系统中，灌注压快速恢复后可能会出现压力突破现象。
