1997 Fiscal Year Final Research Report Summary
Study on the hypoxic glucose output in primary cultured rat hepatocytes
| Project/Area Number |
07671664
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
MORIWAKI Katsuyuki Hiroshima University, Medical Hospital Assistant Professor, 医学部・附属病院, 講師 (30157937)
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| Co-Investigator(Kenkyū-buntansha) |
SHIROYAMA Kazuhisa Hiroshima University, Medical Hospital, Research Associate, 医学部・附属病院, 助手 (30284201)
TANAKA Hiroyuki Hiroshima Univeristy, Medical Hospital, Research Associate, 医学部・附属病院, 助手 (10274086)
YUGE Osafumi Hiroshima University, School of Medicine Professor, 医学部, 教授 (40034128)
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| Project Period (FY) |
1995 – 1997
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| Keywords | Primary cultured rat hepatocytes / Hypoxia / Glucose Metabolism / Lactate Metabolism / Calcium / Dopamine / Volatile Anesthetics |
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| Research Abstract |
Using primary cultured rat hepatocytes, we obtained following results :
1. Fundamental studies on the nature of hypoxic glucose output :
Lactate output was also increased when thehypoxic glucose output increased in the cultured hepatocytes. On the other hand, catecholamines (adrenaline, phenylephrine, isoproterenol) decreased lactate release from the hepatocytes, which might indicate increased uptake of lactate to the hepatocytes. The glucose output from the hepatocytes induced by phenylephrine or isoproterenol was enhanced additively by the concomitant exposure to hypoxia. In addition, hypoxic glucose release was alleviated by exchanging the medium containing calcium to one which contains no calciuim (chileted with EDTA). This finding may suggest hypoxic glucose output is dependent on the inflow of calcium to the hepatocytes to the hepatocytes.
2. Studies on the hypoxic injury of the hepatocytes :
Histological findings : Prolonged hypoxia caused condensation of nuclei and disappearance of the nucleoles, the morphological change of which was positively correlated with leakage of lactate dehydrogenase from the hepatocytes. Glycogen-rich hepatocytes tolerateted well in the hypoxic condition, while glycogen-poor hepatocytes were labile to hypoxia.
3. Pharmacological studies on the effects of agents on the glucose and lactate output under aerobic condition : Volatile anesthetics including halothane, isoflurane and sevoflurane enhanced glucose and lactate output from the hepatocytes in the dose-dependent manner. High dose of dopamine enhanced glucose release from the hepatocytes via activation of beta-receptors.
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