1999 Fiscal Year Final Research Report Summary
Histochemical Study on Onset and Recovery Mechanism of Hepatic Injury Induced by Inhalation Anesthesia in Rats.
| Project/Area Number |
10671415
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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 | Okayama University |
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Principal Investigator |
YAMADA Teruo Medical School, Okayama University Assistant, 医学部, 助手 (00033225)
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| Co-Investigator(Kenkyū-buntansha) |
NOMURA Takako Medical School, Okayama University Assistant, 医学部, 助手 (20116437)
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| Project Period (FY) |
1998 – 1999
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| Keywords | histology / immunohistology / in situ hybridization / inhalation anesthetic / hepatic injury / apoptosis |
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| Research Abstract |
The liver was histochemically examined to study each effect of enflurane (E) , halothane (H) , isoflurane (I), and sevoflurane (S) in phenobarbital-treated (PB-group) and non-treated (N-group) rats. Under 100, 21 and 10% oxygen, rats were exposed to four anesthetics at 1 MAC, respectively, for 2h and the liver was removed at fixed intervals until 7 days after the exposure. Embedded in paraffin and sliced, the liver was stained by various ways of staining to study time-course changes in lobular cell structure. Marked lobular cell change was found only in PB-group under 10% oxygen, while under any other condition no or a little but soon recoverable change was found after the exposure. In PB-group, the liver tissues exposed to each anesthetic were negatively stained with PAS in 1/3 to 2/3 area from the central vein to the portal vein and rRNA disappeared soon after the exposure. The cells in the area negatively stained with PAS degenerated into vacuoles from 12h to 2 days after the exposure. By 7 days after the exposure, the vacuoles disappeared recovering to the normal lobular structure. No anesthetics induced cell proliferation until 7 days and apoptosis dispersed around the vacuoles 1 to 2 days after the exposure. Infiltrated cells appearing in the degenerated area were of macrophage. The degree of cell degeneration induced by each anesthetic showed the following order : H> E > I> S.As to the cause of hepatic injury after inhalation anesthesia, various theories have been reported, but from our results, the main cause is considered that each anesthetic extremely decreases hepatic blood flow volume resulting in the state of ischemia in the central vein area. As to the recovery mechanism, it is considered that after degenerated cells are removed to the central vein by hepatic blood flow, the cells in the portal vein area are rearranged along the hepatic cell cords.
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