Keller T S, McGillicuddy J E, LaBond V A, Kindt G W
J Surg Res. 1985 Nov;39(5):420-32. doi: 10.1016/0022-4804(85)90096-4.
Intravascular volume expansion has been employed successfully for treatment of ischemic stroke from cerebral vasospasm and from cerebrovascular occlusive disease. The physiologic mechanism responsible for this success has not previously been delineated in controlled experimentation. The objective of this investigation was to delineate the effects of cardiac output and of hemodilution in a primate model of focal cerebral ischemia. Two groups of anesthetized rhesus monkeys received extensive cardiovascular monitoring, and local cerebral blood flow (lCBF) was determined in both ischemic and nonischemic brain regions by the hydrogen clearance method. Both groups were subjected to unilateral middle cerebral artery occlusion. One group then underwent blood volume expansion with Dextran 40 (cardiac output augmentation), and one group underwent isovolemic hemodilution with Dextran 40, cardiac output being maintained constant. Significant increases in lCBF occurred in ischemic regions only and occurred only in response to augmentation of cardiac output. Isovolemic hemodilution failed to produce any changes in lCBF. This investigation indicates that ischemic brain regions are selectively vulnerable to alterations in cardiac output, these effects being independent of alterations in blood pressure. Blood viscosity changes may play only a minor role. This study strongly suggests an important role of intravascular volume expansion and cardiac output augmentation in treatment of acute ischemic stroke.
血管内容量扩张已成功用于治疗由脑血管痉挛和脑血管闭塞性疾病引起的缺血性中风。此前，在对照实验中尚未明确导致这种成功的生理机制。本研究的目的是在灵长类动物局灶性脑缺血模型中明确心输出量和血液稀释的影响。两组麻醉的恒河猴接受了广泛的心血管监测，并通过氢清除法测定了缺血和非缺血脑区的局部脑血流量（lCBF）。两组均接受单侧大脑中动脉闭塞。一组随后用右旋糖酐40进行血容量扩张（增加心输出量），另一组用右旋糖酐40进行等容血液稀释，心输出量保持恒定。仅在缺血区域lCBF出现显著增加，且仅在响应心输出量增加时出现。等容血液稀释未能使lCBF发生任何变化。本研究表明，缺血脑区对心输出量的改变具有选择性易损性，这些影响独立于血压的改变。血液粘度变化可能仅起次要作用。本研究强烈提示血管内容量扩张和心输出量增加在急性缺血性中风治疗中具有重要作用。
