Products of hemolysis in the subarachnoid space inducing spreading ischemia in the cortex and focal necrosis in rats: a model for delayed ischemic neurological deficits after subarachnoid hemorrhage?
作者： Jens P. Dreier , Natalie Ebert , Josef Priller , Dirk Megow , Ute Lindauer
DOI: 10.3171/JNS.2000.93.4.0658
关键词: Cerebral blood flow 、 Vasoconstriction 、 Glial fibrillary acidic protein 、 Anesthesia 、 Medicine 、 Vasospasm 、 Subarachnoid space 、 Ischemia 、 Pathology 、 Subarachnoid hemorrhage 、 Brain damage
摘要: Object. The pathogenesis of delayed ischemic neurological deficits after subarachnoid hemorrhage has been related to products hemolysis. Topical brain superfusion artificial cerebrospinal fluid (ACSF) containing the hemolysis K+ and hemoglobin (Hb) was previously shown induce ischemia in rats. Superimposed on a slow vasospastic reaction, events represent spreading depolarizations neuronal—glial network that trigger acute vasoconstriction. purpose present study investigate whether such ischemias cortex lead damage. Methods. A cranial window implanted 31 Cerebral blood flow (CBF) measured using laser Doppler flowmetry, direct current (DC) potentials were recorded. ACSF superfused topically over brain. Rats assigned five groups representing different compositions. Analyses included classic histochemical immunohistochemical studies (glial fibrillary acidic protein ionized cal...
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