EXPERIMENTAL BRAIN INFARCTS IN CATS .2. ISCHEMIC BRAIN EDEMA
EXPERIMENTAL BRAIN INFARCTS IN CATS .2. ISCHEMIC BRAIN EDEMA
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DOI：
10.1161/01.str.11.6.593
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发表时间：
1980-01-01
期刊：
影响因子：
8.3
通讯作者：
HOSSMANN, KA
中科院分区：
文献类型：
--
作者：
SCHUIER, FJ;HOSSMANN, KA
在猫，缺血性脑水肿的早期发展进行了研究后1至4小时，经眶闭塞左侧大脑中动脉（MCA）。比较了两组动物：MCA区域的血流量降低到10-15 ml/100 g/min阈值以下的动物（严重缺血）和血流量保持在该水平以上的动物（非严重缺血）。在严重缺血的动物中，MCA区域皮质中的水含量从80.7 ± 0.001增加到80.7 ± 0.001。0.4至83.0 ±。0.3体积%（平均值±. SE）。水肿与组织渗透压增加16-22 mosm/kg湿重，和钠从262 ± 1升高有关。9到454 .+-. 13毫当量/千克干重K值从442 ± 0.01降低。20到305 .+-. 32 meq/kg干重Na/K比值从0.60 ±. 0.03到1.55 .+-。0.17.水和电解质紊乱伴随着细胞外液向细胞内室的主要转移，如皮质阻抗在2小时内从282欧姆/厘米增加到660欧姆/厘米所证明的。根据麦克斯韦方程，这反映了细胞外间隙从19.8%变窄到11.4%。使用感应传感器连续监测脑体积;肿胀在血管闭塞的几分钟内开始;在整个4小时观察期内持续。在此期间，血脑屏障保持完整，证据是没有伊文思蓝染色。水肿与能量产生代谢紊乱有关，但与乳酸或高能磷酸盐浓度无严格相关性。在没有严重缺血的动物中，即，其中血流量保持> 10-15 ml/100 g/min，尽管脑的能量状态明显恶化，但没有水肿。在临界和非临界缺血动物的边界区、大脑后动脉区域和对侧半球也不存在水肿。大脑中动脉闭塞后的早期缺血性脑水肿是细胞毒性类型的;它在低于10-15 ml/100 g/min的流速下发展，并且它与大脑的能量状态没有严格相关性。
In cats, the early development of ischemic brain edema was studied 1 to 4 h after transorbital occlusion of the left middle cerebral artery (MCA). Two groups of animals were compared: those in which blood flow in the territory of the MCA decreased below the threshold of 10-15 ml/100 g per min (critical ischemia) and those in which it remained above this level (non-critical ischemia). In animals with critical ischemia, water content in the cortex of the MCA territory increased from 80.7 .+-. 0.4 to 83.0 .+-. 0.3 vol % (means .+-. SE) within 4 h. Edema was associated with an increase in tissue osmolality by 16-22 mosm/kg wet wt, and a rise of sodium from 262 .+-. 9 to 454 .+-. 13 meq/kg d.w. and a decrease of K from 442 .+-. 20 to 305 .+-. 32 meq/kg dry wt. The Na/K ratio rose from 0.60 .+-. 0.03 to 1.55 .+-. 0.17. The water and electrolyte disturbances were accompanied by a major shift of extracellular fluid into the intracellular compartment, as evidence by the increase in cortical impedance from 282 to 660 ohm/cm within 2 h. According to the Maxwell equation, this reflects a narrowing of the extracellular space from 19.8 to 11.4%. Brain volume was continuously monitored using an induction transducer; swelling began within a few minutes of vascular occlusion; it continued throughout the 4 h observation period. During this time, the blood-brain barrier remained intact as evidence by the absence of Evans blue staining. Edema was associated with disturbances of the energy producing metabolism, but there was no strict correlation with lactate or the concentration of high energy phosphates. In animals without critical ischemia, i.e., in which blood flow remained > 10-15 ml/100 g per min, edema was absent despite a distinct deterioration of the energy state of the brain. Edema was also absent in the border zone, in the territory of the posterior cerebral artery and in the contralateral hemisphere of animals with critical and non-critical ischemia. The early ischemic brain edema following middle cerebral artery occlusion is of the cytotoxic type; it develops at a flow rate below 10-15 ml/100 g per min and it is not strictly correlated with the energy state of the brain.