高血糖与脑缺血的血管效应

Hyperglycemia and the vascular effects of cerebral ischemia.

作者信息

Kawai N, Keep R F, Betz A L

机构信息

Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor 48109-0532, USA.

出版信息

Stroke. 1997 Jan;28(1):149-54. doi: 10.1161/01.str.28.1.149.

DOI:10.1161/01.str.28.1.149

PMID:8996504

Abstract

BACKGROUND AND PURPOSE

A well-demarcated infarct was observed after 4 hours of rat middle cerebral artery (MCA) occlusion with xylazine/ketamine but not pentobarbital or isoflurane anesthesia. This study examined whether this reflected vascular changes and, because xylazine induces hyperglycemia, whether glucose could cause similar vascular effects in cerebral ischemia.

METHODS

To examine the effects of anesthetics, rats were anesthetized for thread occlusion of the MCA with either xylazine/ketamine, pentobarbital, or isoflurane. To evaluate the effects of glycemia, acute hyperglycemia was induced by glucose injection. In both experiments, cerebral plasma volume (CPV) was determined using 3H-inulin after 4 hours of permanent occlusion, and cerebral blood flow was measured using [14C]iodoantipyrine following 2 hours of reperfusion after 2 or 4 hours of occlusion. The presence of cerebral hemorrhage after reperfusion was checked macroscopically and infarct volume with 2,3,5-triphenyltetrazolium staining.

RESULTS

The ischemic CPV was about 50% of the contralateral values with xylazine/ketamine but not with the other anesthetics. On reperfusion, ischemic cerebral blood flow with xylazine/ketamine anesthesia was approximately half that with pentobarbital. Use of xylazine/ketamine also resulted in more frequent hemorrhagic infarcts and a larger infarct volume. Induced hyperglycemia resulted in a CPV decrease in the ischemic compared with nonischemic tissue (4.0 +/- 0.5 versus 7.4 +/- 0.2 microL/g; P < .001). Hyperglycemia also caused poor reperfusion and increased the occurrence of hemorrhagic infarction (hyperglycemia, 15 of 20; normoglycemia, 1 of 11; P < .01).

CONCLUSIONS

Hyperglycemia induces marked cerebrovascular changes, both during ischemia and during reperfusion, that may exacerbate tissue damage. Change in CPV during ischemia may be a useful clinical indicator in predicting poor hemodynamic recovery and occurrence of hemorrhagic infarction after reperfusion therapy.

摘要

背景与目的

用赛拉嗪/氯胺酮麻醉大鼠大脑中动脉（MCA）4小时后可观察到界限清晰的梗死灶，而戊巴比妥或异氟烷麻醉则未出现此现象。本研究旨在探讨这是否反映了血管变化，以及由于赛拉嗪可诱发高血糖，葡萄糖在脑缺血时是否会产生类似的血管效应。

方法

为研究麻醉剂的作用，用赛拉嗪/氯胺酮、戊巴比妥或异氟烷麻醉大鼠，然后用线栓法阻塞MCA。为评估血糖水平的影响，通过注射葡萄糖诱导急性高血糖。在这两个实验中，永久性阻塞4小时后用3H-菊粉测定脑血浆容量（CPV），阻塞2或4小时后再灌注2小时，用[14C]碘安替比林测量脑血流量。再灌注后肉眼检查脑出血情况，并用2,3,5-三苯基四氮唑染色法测量梗死体积。

结果

赛拉嗪/氯胺酮麻醉时，缺血侧CPV约为对侧值的50%，而其他麻醉剂则无此现象。再灌注时，赛拉嗪/氯胺酮麻醉下的缺血脑血流量约为戊巴比妥麻醉下的一半。使用赛拉嗪/氯胺酮还导致出血性梗死更频繁，梗死体积更大。与非缺血组织相比，诱导高血糖导致缺血组织CPV降低（4.0±0.5对7.4±0.2微升/克；P<.001）。高血糖还导致再灌注不佳，并增加出血性梗死的发生率（高血糖组，20例中有15例；正常血糖组，11例中有1例；P<.01）。