Sato H, Seki H, Ogawa A, Yoshimoto T, Suzuki J
No To Shinkei. 1986 Aug;38(8):773-9.
In order to elucidate the relationship between the degree of autoregulatory loss and the intensity or the duration of ischemia, and the difference of locations in and around the ischemic focus, we used the canine thalamic infarction model and studied the sequential changes of rCBF and autoregulation during 6 hours following vascular occlusion. The value of rCBF was measured by the hydrogen clearance method and autoregulation was tested by raising the blood pressure with drip infusion of angiotensin II. In the center of ischemic focus, autoregulation was impaired after 1, 3 and 5 hours following occlusion in the animals with moderate ischemia. In the animals with mild and severe ischemia, autoregulation was preserved during occlusion, but in the latter we thought it false autoregulation. In the periphery of infarctic focus with severe ischemia, autoregulation was impaired after 3 and 5 hours following occlusion. Outside of the infarctic focus with severe ischemia, autoregulation was preserved during occlusion, but in 2 of 6 animals rCBF decreased despite of raising blood pressure and it was thought to be paradoxical response.
为了阐明自动调节功能丧失程度与缺血强度或持续时间之间的关系,以及缺血灶及其周围部位的差异,我们使用犬丘脑梗死模型,研究血管闭塞后6小时内局部脑血流量(rCBF)和自动调节功能的连续变化。rCBF值采用氢清除法测量,自动调节功能通过静脉滴注血管紧张素II升高血压来测试。在中度缺血的动物中,闭塞后1、3和5小时,缺血灶中心的自动调节功能受损。在轻度和重度缺血的动物中,闭塞期间自动调节功能得以保留,但在重度缺血动物中,我们认为这是假性自动调节。在重度缺血梗死灶周边,闭塞后3和5小时自动调节功能受损。在重度缺血梗死灶外,闭塞期间自动调节功能得以保留,但6只动物中有2只尽管血压升高,rCBF仍下降,这被认为是反常反应。