Inhibition of iNOS with 1400W improves contractile function and alters nos gene and protein expression in reperfused skeletal muscle

This study examined the effects of 1400W, an inhibitor of inducible nitric oxide (iNOS), on contractile function and iNOS expression in reperfused skeletal muscle. The right extensor digitorum longus (EDL) muscle of 104 rats underwent a sham operation or 3‐h ischemia followed by 3‐h or 24‐h reperfus...

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Published in:Microsurgery 2004, Vol.24 (4), p.324-331
Main Authors: Patel, Prerana, Qi, Wen-Ning, Allen, Diane M., Chen, Long-En, Seaber, Anthony V., Stamler, Jonathan S., Urbaniak, James R.
Format: Article
Language:English
Subjects:
Amidines - pharmacology
Animals
Benzylamines - pharmacology
Biological and medical sciences
Enzyme Inhibitors - pharmacology
Female
Gene Expression
General aspects
Medical sciences
Muscle Contraction - drug effects
Muscle Contraction - physiology
Muscle, Skeletal - drug effects
Muscle, Skeletal - physiology
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase - physiology
Nitric Oxide Synthase Type II
Rats
Rats, Sprague-Dawley
Reperfusion Injury - drug therapy
Reperfusion Injury - enzymology
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Summary:This study examined the effects of 1400W, an inhibitor of inducible nitric oxide (iNOS), on contractile function and iNOS expression in reperfused skeletal muscle. The right extensor digitorum longus (EDL) muscle of 104 rats underwent a sham operation or 3‐h ischemia followed by 3‐h or 24‐h reperfusion (I/R). Rats received 3 mg/kg 1400W, 10 mg/kg 1400W, or water subcutaneously. Results showed that EDL contractile function in both 1400W‐treated groups significantly outperformed the controls at 24‐h but not at 3‐h reperfusion. Although iNOS expression increased in all three I/R groups during reperfusion, a significantly smaller increase was found in 1400W‐treated muscles after 3‐h reperfusion, and more dramatically so after 24‐h reperfusion. Our results indicate that inhibition of iNOS preserved the contractile function in reperfused skeletal muscle, perhaps via downregulating iNOS expression. Protection by 1400W at 24‐h reperfusion suggests that the role of iNOS in exaggerating reperfusion injury is more prominent in the later stages of injury. © 2004 Wiley‐Liss, Inc.
ISSN:0738-1085
1098-2752
DOI:10.1002/micr.20029