| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1990: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1989: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
It has been known that during a reperfusion period following transient ischemia cerebral blood flow remarkably increases from the pre-ischemic level. Although this post-ischemic hyperemia can occur in clinical situations such as cerebrovacs ular surgery, neither pathophysiologic significance of this phenomenon nor effects of therapeutic measures to suppress hyperemia have been extensively studied. Therefore, we examined the influences of induced hypotension during the immediate post-ischemic period upon cerebral blood flow, blood-brain barrier function, and neurologic outcome. (Methods) The middle cerebral artery was exposed by a transorbital approach using a surgical microscope in 27 adult cats anesthetized and mechanically ventilated. In the first series of experiment, the regional Cerebral Blood Flow (rCBF ; hydrogen clearance method), extracellular potassium ion (Kec ; electrometer technique), and electroencephalogram were recorded, while the middle cerebral artery was occluded for
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three hours and then released for two hours. Following a reperfusion period of two hours, Evans blue penetration index was calculated in slices of fixed brain samples. In the second series of experiment, neurologic deficits were scored at 48 hours after a 3 hours cerebral ischemia. In both series, animals were grouped according to the method of hemodynamic management at reperfusion ; without specific control=A, A', controlled with halothane=B, B', and controlled with pentobarbital=C, C'. (Results) Mean arterial blood pressure was significantly reduced by 20 to 35mmHgin groups B/B' and C/C', compared to groups A/A'. However, post-ischemic rCBF was not significantly different between groups. The mean Evans blue penetration index was 232, 93, and 26, in groups A, B, and C, respectively. The difference of the index between groups A and C was statistically significant. Neurological deficit score was significantly greater in group A' than in groups B' and C'. (Discussion) These results suggest that hemodynamic management by induced hypotension reduces penetration of plasma protein, and hence the development of vasogenic brain edema at reperfusion following a transient cerebral ischemia. Neurologic outcome was also improved by induced hypotension. However, hyperemic responses were not always suppressed by reduction of systemic blood pressure. Further studies were necessary to clarify the relationship between blood pressure and rCBF at the immediate reperfusion and the effects of other hypotensive agents or hypocapnia. Less
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