| Selective iNOS Inhibition Attenuates Skeletal Muscle Reperfusion Injury |
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Jong Woong Park, M.D.*, Kwang Suk Lee, M.D., Sung Kon Kim, M.D., Jung Ho Park, M.D., Joon Ho Wang, M.D., Woo Joo Jeon, M.D., Jeong Il Lee, M.D. |
| 선택적 iNOS 억제에 의한 골격근 재관류 손상의 감소 |
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박종웅*, 이광석, 김성곤, 박정호, 왕준호, 전우주, 이정일 |
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| Abstract |
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The purpose of this study is to determine the effects of selective inducible nitric oxide synthase (iNOS) inhibitor N-[3-aminomethyl]benzyl]acetamidine (1400W) on the reperfused cremaster muscle. The extracellular superoxide dismutase knockout (EC-SOD-/-) mice was used to make the experimental window for ischemia-reperfusion injury. The muscle was exposed to 4.5 h of ischemia followed by 90 min of reperfusion and the mice received either 3 mg/kg of 1400W or the same amount of phosphate buffered saline (PBS) subcutaneously at 10 min before the start of reperfusion. The results showed that 1400W treatment markedly improved the recovery of the vessel diameter and blood flow in the reperfused cremaster muscle compared to that of PBS group. Histological examination showed reduced edema in the interstitium and muscle fiber, and reduced nitrotyrosine formation (a marker of total peroxinitrite (ONOO-)) in 1400W-treated muscle compared to PBS. Our results suggest that iNOS and ONOO- products are involved in skeletal muscle I/R injury. Reduced I/R injury by using selective inhibition of iNOS is perhaps via limiting cytotoxic ONOO- generation, a reaction product of nitric oxide (NO) and superoxide anion (O2 -). Thus, inhibition of iNOS appears to be a good treatment strategy in reducing clinical I/R injury. |
| Key Words:
iNOS inhibitor, Extracellular SOD, Reperfusion, Muscle, Mouse |
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