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溶血在实验性脑血管痉挛中作用的证据。

Evidence of the role of hemolysis in experimental cerebral vasospasm.

作者信息

Peterson J W, Roussos L, Kwun B D, Hackett J D, Owen C J, Zervas N T

机构信息

Laboratory for Cerebrovascular Biophysics, Massachusetts General Hospital, Boston.

出版信息

J Neurosurg. 1990 May;72(5):775-81. doi: 10.3171/jns.1990.72.5.0775.

DOI:10.3171/jns.1990.72.5.0775
PMID:2324801
Abstract

The short-term (less than or equal to 72-hour) reaction to subarachnoid injections of various blood components was determined in a canine model of cerebral vasospasm. Platelet-rich plasma (PRP) formed durable clots in the basal cistern surrounding the basilar artery and provoked no vascular reaction in 72 hours or more. Freshly isolated autologous erythrocytes resuspended in PRP likewise provoked no vasoconstriction in 72 hours although a second injection of fresh erythrocytes in PRP induced significant reaction, as in the conventional "double subarachnoid hemorrhage (SAH)" canine model. Hemolysate of fresh erythrocytes led to a severe immediate vascular reaction after introduction into the basal cistern using PRP as the carrier/clotting medium, as did the injection of intact erythrocytes incubated ex vivo for 72 hours. Resolution of the initial reaction was rapid for hemolysate, but slow and (depending on hematocrit) incomplete for intact "aged" erythrocytes. In vitro measurements of erythrocyte lysis in these media and histological examination indicate that the production of erythrocyte lysate was responsible for the vascular reaction observed, suggesting that the rate of lysis of erythrocytes in the subarachnoid clot is a major factor in the genesis of vasospasm after SAH.

摘要

在犬脑血管痉挛模型中,确定了蛛网膜下腔注射各种血液成分的短期(小于或等于72小时)反应。富含血小板的血浆(PRP)在基底动脉周围的基底池中形成持久的凝块,在72小时或更长时间内未引发血管反应。重新悬浮在PRP中的新鲜分离的自体红细胞在72小时内同样未引发血管收缩,尽管在PRP中第二次注射新鲜红细胞会引发显著反应,就像传统的“双蛛网膜下腔出血(SAH)”犬模型一样。使用PRP作为载体/凝血介质将新鲜红细胞的溶血产物引入基底池后,会导致严重的即时血管反应,将离体孵育72小时的完整红细胞注射到基底池后也会出现这种情况。溶血产物引发的初始反应消退迅速,但完整的“老化”红细胞引发的反应消退缓慢且(取决于血细胞比容)不完全。在这些介质中对红细胞裂解的体外测量和组织学检查表明,观察到的血管反应是由红细胞裂解产物的产生引起的,这表明蛛网膜下腔凝块中红细胞的裂解速率是SAH后血管痉挛发生的一个主要因素。

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