2000 Fiscal Year Final Research Report Summary
EFFECTS OF HYPOTHERMIA ON THE INDUCTION OF NO SYNTHASE EVOKED BY CYTOKINE IN VASCULAR SMOOTH MUSCLE
Project/Area Number |
11671519
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
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Research Institution | WAKAYAMA MEDICAL COLLEGE |
Principal Investigator |
MAEDA Hiroshi WAKAYAMA MEDICAL COLLEGE, DEPARTMENT OF ANESTHESIOLOGY, INSTRUCTOR, 医学部, 助手 (80199629)
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Co-Investigator(Kenkyū-buntansha) |
HATANO Yoshio WAKAYAMA MEDICAL COLLEGE, DEPARTMENT OF ANESTHESIOLOGY, PROFESSOR AND CHAIRMAN, 医学部, 教授 (70115913)
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Project Period (FY) |
1999 – 2000
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Keywords | VASCULAR SMOOTH MUSCLE / CYTOKINE / NO SYNTHASE / HYPOTHERMIA |
Research Abstract |
The purpose of this study was to clarify the effect of hypothermia on IL-1β evoked iNOS induction in vascular smooth muscle. Exposure of rat aortic rings without endothelium to IL-1β for 5h in 37℃ Krebs Ringer solution significantly attenuated the contractile responses to phenylephrine and KCl. These attenuations were reduced when exposed to IL-1β for 5h in 27℃ Krebs Rnger solution. Exposure of the endothelium-denuded rat aorta to IL-1β for 5 h in 37℃ Krebs Ringer solution caused an increase in the tissue cGMP contents. The levels of cGMP measured in aortic strips that were exposed to IL-1β for 5h in 27℃ Krebs Ringer solution were significantly lower than those in 37℃. The expressions of iNOS mRNA and iNOS protein evoked by the exposure to IL-1β for 5h in 37℃ Krebs Ringer solution were attenuated by the exposure to IL-1β in 27℃. The present study demonstrated that hypothermia attenuated the IL-1β evoked iNOS induction in vascular smooth muscle. These results suggest that iNOS induction may participate in the mechanism of ischemic brain damage and that the attenuation of iNOS induction may contribute the brain protection with hypothermia.
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