Effects of anesthetics on the renal dysfunction induced by ischemia
Project/Area Number |
03670733
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
麻酔学
|
Research Institution | Kagoshima University |
Principal Investigator |
YOSHIMURA Nozomu Kagoshima University, School of Medicine, Professor, 医学部, 教授 (60041399)
|
Co-Investigator(Kenkyū-buntansha) |
SAMESHIMA Teruko Kagoshima University, School of Medicine, Research Associates, 医学部, 助手 (10041328)
|
Project Period (FY) |
1991 – 1992
|
Project Status |
Completed (Fiscal Year 1992)
|
Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
Keywords | Halogenated anesthetics / Intravenous anesthetics / Renal ischemia / Renal dysfunction / Allopurinol |
Research Abstract |
Effects of halogenated and intravenous anesthetics on cell injury following renal ischemia were studied. We also investigated the effects of allopurinol and glutathione on renal dysfunction following renal ischemia. Male Wister rats were divided into treatment groups. The left renal artery was dissected and clipped under each anesthesia for 30 min. Anesthesia was maintained for 90 min after release of the clip. As halogenated anesthetics. 1.3MAC of halothane, enflurane, isoflurane, and sevoflurane were used. As intravenous anestyetics, pentobarbital and fentanyl were administered at the concentration of 30mg/kg and 10 mug/kg, respectively. 3mg/kg of allopurinol and 100mg/kg of glutathione were administered before clipping the renal artery under 1.3MAC enflurane anesthesia. 24 hours after discontinuation of anesthesia, the treated kidney was examined for necrosis. NAG and _<gamma>GTP in urine and kidney were determined at the completion of anesthesia and 24 hours after discontinuation o
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f anesthesia. Plasma inorganic fluoride, BUN, creatinine, lysosomal enzymes, sGOT were determined at the same times. The degree of necrosis of halogenated anesthetics was enflurane > sevoflurane > halothane > isoflurane. The degree of necrosis was higher in pentobarbital and fentanyl groups than in enflurane group. Urinary NAG and _<gamma>GTP were markedly elevated by ischemia. NAG and _<gamma>GTP in kidney were decreased by ischemia. Plasma BUN, creatinine, lysosomal enzymes, sGOT, and sGPT were significantly increased after discontinuation of anestesia. Degree of necrosis did not correlated with urinary enzyme activities, plasma BUN and creatinine. Plasma inorganic fluoride was increased in enflurane and sevoflurane. The degree of necrosis was decreased by administration of allopurinol. These results suggested that kidney damage following renal ischemia was most severe in enflurane and least severe after isoflurane anesthesia. Pentobarbital and fentanyl enhanced the renal damage than halogenated anesthetics. Inorganic fluoride did not affect renal injury induced by ischemia. It was suggested that renal ischemia might induce damage to other organs. The renal damage following renal ischemia was decreased by the administration of allopurinol. Less
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Report
(3 results)
Research Products
(4 results)