蛛网膜下腔出血后早期脑损伤的研究进展

Progress in early brain injury after subarachnoid hemorrhage

蛛网膜下腔出血是神经外科常见病,死亡率高,目前国内外对蛛网膜下腔出血后迟发性脑血管痉挛的研究已相当深入,但临床工作发现蛛网膜下腔出血后早期死亡的患者脑组织普遍存在严重的缺血损伤,涉及到迟发性脑血管痉挛出现(3 d^2周)之前脑组织内所发生的病理生理事件,包括脑灌注、微循环变化,基质金属蛋白酶、纤溶酶原激活剂等酶的消化作用导致基底膜IV型胶原蛋白缺失,分布于蛛网膜下腔的血清、富含血小板的血浆促成蛛网膜下腔出血后急性血管收缩,血小板的活化及在微血管内聚集打断脑循环导致脑灌注不足、局部缺血加剧等一系列病理生理学变化。针对这些现象,本文就蛛网膜下腔出血后早期脑损伤的机制及进展做一综述,为未来能更好控制这些继发性事件、有效治疗急性蛛网膜下腔出血提供初步的理论基础依据。

Subarachnoid hemorrhage is a common disease in neurosurgery with a high mortality. Researches on delayed cerebral vasospasm（CVS） after subarachnoid hemorrhage are explored in China at home and abroad. However, clinical work finds patients with early death after SAH. There is a widespread ischemic injury in the brain that involves the pathophysiological events that occur in the brain tissue prior to late onset of cerebral vasospasm （3 days to 2 weeks）.It includs changes in cerebral perfusion, microcirculation, matrix metalloproteinases, digestion of plasminogen activator and other enzymes lead to the loss of type IV collagen in the basilar membrane, distribution in the subarachnoid serum, platelet rich plasma to promote acute vasoconstriction after SAH, platelet activation and aggregation in the microvascular break Cerebral circulation lead to insufficient cerebral perfusion, ischemia and a series of pathophysiological changes. This article reviews the mechanism and progress of EBI after SAH, in order to provide a preliminary theoretical basis for better control of these secondary events and effective treatment of acute SAH in future.