Xi G, Hua Y, Bhasin R R, Ennis S R, Keep R F, Hoff J T
Department of Neurosurgery, University of Michigan, Ann Arbor, USA.
Stroke. 2001 Dec 1;32(12):2932-8. doi: 10.1161/hs1201.099820.
Red blood cell (RBC) lysis contributes to brain edema formation after intracerebral hemorrhage (ICH), and RBC hemolysate (oxyhemoglobin) has been implicated to be a spasminogen in subarachnoid hemorrhage. Whether cerebral ischemia contributes to brain edema formation after ICH remains unclear, however. The aims of this study were to test whether extravasation of RBCs induces cerebral ischemia and/or blood-brain barrier disruption in a rat ICH model characterized by perihematomal brain edema.
In this study, 87 pentobarbital-anesthetized Sprague-Dawley rats were used. In each animal, saline, packed RBCs, or lysed RBCs were injected into the right caudate nucleus. Sham injections served as controls. Regional cerebral blood flow, brain water and ion contents, blood-brain barrier integrity, and plasma volume were measured.
Intraparenchymal infusion of lysed RBCs caused severe brain edema by the first day but did not induce ischemic cerebral blood flows. In contrast, blood-brain barrier permeability increased during the first day after infusion of lysed RBCs (a 3-fold increase) and 3 days after infusion of packed RBCs (a 4-fold increase).
These results suggest that ischemia is not present at 24 or 72 hours after hematoma induction by injection of intact or lysed RBCs. RBC constituents that appear after delayed lysis, however, increase blood-brain barrier permeability, which contributes to edema formation.
红细胞（RBC）溶解在脑出血（ICH）后会促使脑水肿形成，并且红细胞溶血产物（氧合血红蛋白）被认为是蛛网膜下腔出血中的一种致痉原。然而，脑缺血是否会促使脑出血后脑水肿形成仍不清楚。本研究的目的是在以血肿周围脑水肿为特征的大鼠脑出血模型中，检测红细胞外渗是否会诱发脑缺血和/或血脑屏障破坏。
本研究使用了87只戊巴比妥麻醉的Sprague-Dawley大鼠。在每只动物中，将生理盐水、浓缩红细胞或裂解红细胞注入右侧尾状核。假注射作为对照。测量局部脑血流量、脑水和离子含量、血脑屏障完整性以及血浆容量。
脑实质内注入裂解红细胞在第一天就导致严重脑水肿，但未诱发缺血性脑血流。相比之下，注入裂解红细胞后第一天血脑屏障通透性增加（增加3倍），注入浓缩红细胞后3天血脑屏障通透性增加（增加4倍）。
这些结果表明，在注射完整或裂解红细胞诱导血肿后24或72小时不存在缺血情况。然而，延迟溶解后出现的红细胞成分会增加血脑屏障通透性，这有助于水肿形成。
