Immunohistochemical investigation of cerebral ischemia during recirculation
Toshiki Yoshimine, Kazuyoshi Morimoto, Joan M. Brengman, Henry A. Homburger, Heitaro MOGAMI, Takehiko Yanagihara
Abstract
Toshiki Yoshimine, Kazuyoshi Morimoto, Joan M. Brengman, Henry A. Homburger, Heitaro MOGAMI, Takehiko Yanagihara
Abstract
Immunohistochemical methods for the determination of tubulin, creatine kinase BB-isoenzyme, and astroprotein-glial fibrillary acidic protein were used to investigate recovery of the ischemic lesion after temporary occlusion of a common carotid artery in the gerbil and the evolution of the postischemic lesion following reperfusion. One group of gerbils was followed from 15 minutes to one month after an ischemic period of 30 minutes, and another group was examined after 7 days following an ischemic period of 5 to 30 minutes. It was found that the postischemic lesion, visualized as loss of the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme, evolved within 60 minutes after reperfusion in the hippocampus and cerebral cortex and within 3 hours in the caudoputamen and thalamus. Resolution of the preexisting ischemic lesion was possible only after an ischemic period of less than 10 minutes in the cerebral cortex and caudoputamen and less than 15 minutes in the thalamus. In the CA1-CA2 region of the hippocampus, the ischemic lesion already existed after an ischemic period of 5 minutes and was mostly irreversible. The immunohistochemical method of testing for different cellular and subcellular components was very useful for investigation of cerebral ischemia and may also be advantageous for investigation of other pathophysiological conditions of the nervous system.
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Immunohistochemical methods for the determination of tubulin, creatine kinase BB-isoenzyme, and astroprotein-glial fibrillary acidic protein were used to investigate recovery of the ischemic lesion after temporary occlusion of a common carotid artery in the gerbil and the evolution of the postischemic lesion following reperfusion. One group of gerbils was followed from 15 minutes to one month after an ischemic period of 30 minutes, and another group was examined after 7 days following an ischemic period of 5 to 30 minutes. It was found that the postischemic lesion, visualized as loss of the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme, evolved within 60 minutes after reperfusion in the hippocampus and cerebral cortex and within 3 hours in the caudoputamen and thalamus. Resolution of the preexisting ischemic lesion was possible only after an ischemic period of less than 10 minutes in the cerebral cortex and caudoputamen and less than 15 minutes in the thalamus. In the CA1-CA2 region of the hippocampus, the ischemic lesion already existed after an ischemic period of 5 minutes and was mostly irreversible. The immunohistochemical method of testing for different cellular and subcellular components was very useful for investigation of cerebral ischemia and may also be advantageous for investigation of other pathophysiological conditions of the nervous system.
Key concepts: Medicine, Gerbil, Ischemia, Lesion, Hippocampus, Thalamus, Immunohistochemistry, Pathology