Biochemical Alterations in the Anoxic-Ischemic Lesion of Rat Brain

作者：Nancy R. Clendenon, Nicholas Justin Allen, Toru Komatsu, Leopold Liss, Wanda A. Gordon, Karl Heimberger · 发表于：Archives of Neurology · 年份：1971 · DOI：10.1001/archneur.1971.00490050066006 · 被引用次数：52 · 研究领域：Mitochondrial Function and Pathology、Neuroscience and Neuropharmacology Research、Calpain Protease Function and Regulation

The combined effects of unilateral vascular occlusion and anoxia resulted in a high yield of cerebral infarctions in rats with clinical evidence of hemiplegia. Our data support the hypothesis of a complex, consecutive series of biochemical events, gradually developing and culminating in infarction. Accumulation of fluid was detected by 15 minutes and evidence for mitochondrial fragmentation by one hour following the anoxic-ischemic insult. Lysosomal enzyme release either was minimal or occurred after three hours and would not appear to be a decisive factor in the pathogenesis of cell injury in nervous tissue. Complex alterations in glycogen metabolism were demonstrated on the infarcted side and in the adjacent cortex of the contralateral hemisphere. Endothelial swelling was noted at the small arteriole and capillary level and may contribute to the development and the severity of the injury.