Erythrocytes and delayed brain edema formation following intracerebral hemorrhage in rats
Erythrocytes and delayed brain edema formation following intracerebral hemorrhage in rats
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DOI：
10.3171/jns.1998.89.6.0991
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发表时间：
1998-12-01
影响因子：
4.1
通讯作者：
Hoff, JT
中科院分区：
文献类型：
--
作者：
Xi, GH;Keep, RF;Hoff, JT
Object.自发性脑出血（ICH）后脑水肿形成的机制尚不清楚。在以前的研究中，在将浓缩红细胞（RBC）输注到大鼠或猪的大脑中后24小时，没有发现明显的水肿形成;然而，有证据表明血红蛋白可能具有神经毒性。在这项研究中，作者重新检查了红细胞和血红蛋白在ICH后水肿形成中的作用。实验涉及将全血、浓缩RBC、裂解RBC、大鼠血红蛋白或凝血酶输注到Sprague-Dawley大鼠的右侧基底神经节中。在不同时间点处死动物，测定脑水和离子含量。结果表明，输注后24小时，裂解的自体红细胞（而非浓缩红细胞）产生明显的脑水肿，并且这种水肿形成可以通过血红蛋白输注来模拟。虽然输注浓缩的RBC在前2天内没有产生显著的脑水肿，但在输注后3天确实诱导脑含水量显著增加。凝血酶输注后的水肿形成在24至48小时达到峰值。这早于ICH后水肿形成的高峰，提示ICH中存在延迟的、非凝血酶介导的致水肿成分。这些结果表明，RBC在ICH后延迟水肿发展中发挥潜在的重要作用，RBC溶解和血红蛋白毒性可能是治疗干预的有用靶点。
Object. The mechanisms of brain edema formation following spontaneous intracerebral hemorrhage (ICH) are not well understood. In previous studies, no significant edema formation has been found 24 hours after infusion of packed red blood cells (RBCs) into the brain of a rat or pig; however, there is evidence that hemoglobin can be neurotoxic. In this study, the authors reexamined the role of RBCs and hemoglobin in edema formation after ICH.Methods. The experiments involved infusion of whole blood, packed RBCs, lysed RBCs, rat hemoglobin, or thrombin into the right basal ganglia of Sprague-Dawley rats. The animals were killed at different time points and brain water and ion contents were measured. The results showed that lysed autologous erythrocytes, but not packed erythrocytes, produced marked brain edema 24 hours after infusion and that this edema formation could be mimicked by hemoglobin infusion. Although infusion of packed RBCs did not produce dramatic brain edema during the first 2 days, it did induce a marked increase in brain water content 3 days postinfusion. Edema formation following thrombin infusion peaked at 24 to 48 hours. This is earlier than the peak in edema formation that follows ICH, suggesting that there is a delayed, nonthrombin-mediated, edemogenic component of ICH.Conclusions. These results demonstrate that RBCs play a potentially important role in delayed edema development after ICH and that RBC lysis and hemoglobin toxicity may be useful targets for therapeutic intervention.