| Project/Area Number |
12671450
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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 | UNIVERSITY OF TSUKUBA |
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Principal Investigator |
MIYABE Masayuki INSTITUTE OF CLINICAL MEDICINE, UNIVERSITY OF TSUKUBA, ASSOCIATE PROFESSOR, 臨床医学系, 助教授 (60145589)
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| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | HEMORRHAGIC SHOCK / LEUKOCYTE / NO / 白血球接着 / 一酸化窒素 |
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| Research Abstract |
The adhesion of polymorphonuclear leukocytes to the capillary endothelium is one of the key events in the pathophysiology of hemorrhagic shock. SNP was studied for its ability to modulate leukocyte-endothelial cell interactions induced by hemorrhagic shock and reinfusion of blood using intravital microscopy of the rat mesentery. Administration of SNP at a dose of 0.1 μg/kg/min infusion neither significantly decreased mean arterial blood pressure (MABP) nor significantly altered bleedout volumes in hemorrhagic rats, indicating that SNP at this dose did not modify the severity of the shock protocol. Resuscitation from 1 hour hemorrhagic shock (MABP around 45 mm Hg) significantly increased the number of adherent and emigrated leukocytes in the rat mesenteric microcirculation. However, infusion of SNP, started 15 min before hemorrhage and continued over the entire experimental period, markedly reduced the leukocyte adhesion after reinfusion and emigration during hemorrhagic shock and after reinfusion. It is concluded that the NO donor SNP is effective at reducing the leukocyte endothelial interaction after the blood reinfusion following hemorrhagic shock in rats. Implications : The intravenous infusion of 0.1 μg/kg/min of SNP, a dose which does not exert a significant vasodilator effect, reduces leukocyte adhesion and emigration after hemorrhagic shock.
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