| Project/Area Number |
12670545
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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 |
Respiratory organ internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
SHINDOH Chiyohiko College of Medical Sciences, Tohoku University, Professor, 医療技術短期大学部, 教授 (10216228)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Muscle fatigue / ATPase staining / Respiratory muscle failure / サイトカイン |
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| Research Abstract |
(1) Experimental setup : We have made an experimental setup for measurements of diaphragm muscle contractility with an organ bath and a PCR cycler, which we requested for an equipment. Using the experimental setup, we performed an experiment about what effects of cytokines of IL-8, IL-10 and IL-13 on diaphragm muscle.
(2) Effects of IL-8 on diaphragm muscle : After IL-8 (3 μg/kg) was given via tail vein of Wistar rats, we measured force-frequency curves and twitch contractions at 0, 2 and 4 hours. IL-8 decreased significantly the force-frequency curves at 2 and 4 hours, and NO production was observed in type I (slow-twitch) and IIa (oxygenative-fast-twitch) muscle fibers in time-dependently.
(3) Effects of IL-10 and IL-13 on diaphragm muscle : Both IL-10 and IL-13 prevented the decrease of force-frequency curves by endotoxin (30 mg/kg) which was given into peritoneal cavity of animals. They also inhibited NO production performed by NADPH diaphorase staining in the diaphragm muscle fibers.
(4) From these results, it is suggested that IL-8 (a cytokine related to inflammation) causes deterioration of diaphragm muscle function and NO production in diaphragm muscle fibers. However, there is a protective mechanism of IL-10 and IL-13 (Th2 cytokines) to scavenge NO, and prevented diaphragm muscle deterioration induced by endotoxin. The present study suggests that these Th2 cytokines has a possibility of clinical application for treatment of respiratory muscle failure due to septicemia.
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