| Project/Area Number |
13671315
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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 |
Digestive surgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
HAMADA Nobuo Kagoshima University, University Hospital, Faculty of Medicine, assistant professor, 医学部, 講師 (30253868)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Noboru Kagoshima University, University Hospital, Faculty of Medicine, Research Associate, 医学部附属病院, 助手
KOMOKATA Teruo Kagoshima University, University Hospital, Faculty of Medicine, Research Associate, 医学部附属病院, 助手
石崎 直樹 鹿児島大学, 医学部・附属病院, 助手
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Small intestine / Ischemia-reperfusion injury / Ischemic preconditioning / K_<ATP> channel / Ischemic Preconditioning / ATP感受性Kチャンネル |
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| Research Abstract |
While ischemic preconditioning (IP) has been shown to have protective effect for ischemia-reperfusion injury (IRI) in several organ systems, little is known about the effect on intestinal IRI. In this study, we investigated the immediate protective effect of IP on intestinal IRI.
The entire canine small intestine was isolated on a vascular pedicle that consisted of the proximal superior mesenteric artery and vein. Complete intestinal warm ischemia was induced by clamping these vessels. The dogs were randomized into four groups (each n=5) : Group I -control group, animals subjected to 120 min of intestinal ischemia, followed by 240 min of reperfusion. Group II -ischemic preconditioning group (IP) : Before the ischemia reperfusion period (as in group I), animals were subjected to previous ischemic preconditioning with 15 min of ischemia and 15 min of reperfusion. Group III -nicorandil (Nic) treated group, same as group I, but nicorandil, a selective K_<ATP> channel opener, was given to animals with bolus injection of 100 μg/kg/min during the reperfusion. Group IV -glibenclamide (Gli) treated group, same as group II, but 0.3 mg/kg of glibenclamide, selective K_<ATP> channel blocker, was given intravenously 15 min before IPC.
Compared to the control, the preconditioned group reduced CPK and lactate levels in the portal vein, maintained the intestinal mucosal pH (pHi) and attenuated the histological tissue damage after reperfusion. Nic treatment showed better outcome of pHi, and Gli administration attenuated the ischemic preconditioning effect.
These results suggest that IP can protect the intestine from the prolonged ischemia and reperfusion injury and that the K_<ATP> channel plays an important role in this protection mechanism.
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