1990 Fiscal Year Final Research Report Summary
Effects of Anesthetics on the Morphological and Metabolic Changes due to the Hepatic Ischemia.
| Project/Area Number |
01570868
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | Kagoshima University |
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Principal Investigator |
YOSHIMURA Nozomu Kagoshima University, Faculty of Medicine, Professor, 医学部, 教授 (60041399)
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| Co-Investigator(Kenkyū-buntansha) |
SAMESHIMA Teruko Kagoshima University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (10041328)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Hepatotoxicity / Ischemia / Anesthetics / Hypoxia |
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| Research Abstract |
The effect of anesthetics (halothane, isoflurane, enflurane, sevoflurane and pentobarbital) on ischemia produced hepatic cell deterioration was studied in rats whose left lateral and median lobes were clamped by means of a microsurgical clip. Thereafter the effect of reduced glutation on its hepatotoxicity was investigated. After 15 minutes clamping under 30% oxygen, the amount of necrotic areas in the left lateral lobe and serum enzyme activity increased significantly. After 30 minutes clamping, there were more remarkable increases. Halothane and sevoflurane minimized the necrotic areas and suppressed the elevation of serum and lysozomal enzymes, when compared with ischemic alone. However enflurane and isoflurane did not strengthen the hepatotoxicity. The necrotic areas produced by ischemia under 9% oxygen increased more significantly than under 30% oxygen, but serum enzyme levels remained unchanged. Halothane and sevoflurane also had a tendency to protect the ischemia produced hepatotoxicity under 9% oxygen. Hepatic energy levels decreased from ischemia, but were higher in anesthetized groups than in ischemic alone. Pentobarbital minimized the necrotic area, suppressed the elevation of serum and lysozomal enzymes, and maintained hepatic energy levels higher than halothane. The administration of GSH prior to ischemia had a protective effect on ischemia produced hepatic cell deterioration under halothane anesthesia. Hepatic energy levels were significantly higher in the GSH treated group than in halothane anethesia. From these results, it was suggested that anesthetics might have a protective effect on ischemia produced hepatotoxicity and that the administration of GSH which has a favorable effect on energy restoration might be more effective in hepatotoxicity.
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