[Alteration of regional calcium and energy metabolism in ischemic neuronal injury].
To elucidate mechanisms of intra-and postischemic brain damage, regional alterations of calcium and energy metabolism were investigated by histochemical methods. Permanent ischemia of 1 and 3 hours, and temporary ischemia of 15 min, 1 and 3 hours with subsequent recirculation were made in gerbils. In the first of present study, calcium leakage was studied in the permanent ischemia. Abnormal calcium stains were observed in the area where ATP content markedly decreased, and they were already noted in the 15 min ischemia. These calcium stains were mainly seen around the blood vessels, and also seen in the tissue at the border of the ischemic area. Distribution of the calcium stains were more intense in the proximity of the large arteries than their distal portion. Thus the results show calcium leakage from the blood vessels developed in the early stage of ischemia, and such vessels were localized in the area where decrease of perfusion pressure was persisted above the level sufficient for calcium leakage. In the second of present study, regional changes of calcium and energy metabolism were studied in reperfusion of 1 and 3 hours hemispheric ischemia. Although postischemic restoration of brain ATP content varied greatly in different regions, the ATP restoration after the 1 hour ischemia was better than that after the 3 hours ischemia. Abnormal calcium stains were seen in the cortex, the hippocampal Ammon's horn, the ventral postero-lateral thalamic nucleus and the habenula. These calcium stains mainly localized in the neurons, which were different from intraischemic ones. In the third of present study, regional changes of calcium and energy metabolism were studied in the later stage of recirculation after 15 min forebrain ischemia. Although tissue ATP content recovered to normal at 6 hours after the recirculation, it gradually decreased in the hippocampal subiculum-CA1 regions as the recirculation time increased. In the regions of reduced ATP content, an alkaline pH shift and loss of Nissl's staining were noted. Abnormal calcium stains were seen in the cortical neurons in layers 3 and 5-6, the hippocampal Ammon's horn and the ventral postero-lateral thalamic nucleus. The distribution of these calcium stains was almost consistent with that in the second study. In the hippocampal subiculum-CA1 regions, the abnormal calcium stains preceded the alteration of ATP and tissue pH. Abnormality in the calcium staining was also noted in the hippocampal CA3-CA4 regions and the ventral postero-lateral thalamic nucleus, where the decrease of ATP or the histopathological change did not develop.(ABSTRACT TRUNCATED AT 400 WORDS)
Kobayashi
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D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D002118:Calcium / Q000378:metabolism*; D004734:Energy Metabolism; D005849:Gerbillinae; D006651:Histocytochemistry; D009474:Neurons / Q000378:metabolism / Q000473:pathology
D000255:Adenosine Triphosphate; D002118:Calcium