| Project/Area Number |
07670800
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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 |
Circulatory organs internal medicine
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| Research Institution | Wakayama Medical College |
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Principal Investigator |
HANO Takuzo Wakayama Medical College, Medicine, Associate Professor, 医学部, 助教授 (90156381)
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| Co-Investigator(Kenkyū-buntansha) |
BABA Akira Wakayama Medical College, Medicine, Senior Staff, 医学部, 助手 (00228678)
SHIOTANI Masahiko Wakayama Medical College, Medicine, Assistant Professor, 医学部, 講師 (90275355)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | rabbit / reperfusion injury / glomerulus / afferent arterioles / endothelium / calcium antagonist |
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| Research Abstract |
Ischemia reperfusion injury is one of the most important pathophysiological phenomena, which occurs in shock, transplants and other ischemic disease. This study was carried out to determine the mechanisms of ischemia reperfusion injury in microvessels.
After 15-minute ischemia and 30-minute reperfusion, rabbit afferent arterioles (Af-Art) with the glomerulus intact were microdissected from the superficial cortex of the rabbit kidney and perfused in vitro at 60mmHg. Vasoconstrictor action of norepinephirine (NE) and vasodilator action of acetylcholin (Ach) or nicardipine (Nic) were examined. Af-Art were examined with an electron microscope.
Nic 1mg/kg/min was addminstrated intravenously 15 minute before the occulusion of renal artery. Then same protocol was repeated again.
The ischemia reperfusion significantly attenuated the dilation induced by 10^<-5>M Ach 4.7% (n=5) VS 5.4% in controls (n=5)}. However, the response to 5x10^<-7>M NE remained unchanged 4.6% (n=4) VS 6.5% in controls (n=8)}, as did the dilation induced by 10^<-7>M Nic 6.5% (n=7) VS 6.5% in controls (n=7)}. Slight damages were observed in the endothelial cells on electron microscopy. There was no damage to Af-Arts after 20 minutes ischemia only, either functionally or histologically. Pretreatment of Nic could reverse endothelial damage by ischemia reperfusion injury.
We conclude that short period of the ischema reparfusion could induce functional and histological damage to Af-Art. The endothelial cells of microvessels are more susceptible to ischemia reperfusion than smooth muscle cells. Calcium antagonist improve the endothelial damage by ischemia reperfusion injury via calcium channel dependent mechanisms.
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