{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T15:29:11Z","timestamp":1759332551365},"reference-count":48,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2003,12,29]],"date-time":"2003-12-29T00:00:00Z","timestamp":1072656000000},"content-version":"vor","delay-in-days":362,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Microsurgery"],"published-print":{"date-parts":[[2003,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>To determine the role of inhibition of complement activation in the contractile function of skeletal muscle ischemia\u2010reperfusion (I\/R) injury, the rat extensor digitorum longus (EDL) muscles underwent 3 h ischemia and received human C1\u2010esterase inhibitor (C1\u2010INH, 100 IU\/kg), a synthetic C1q A chain peptide with a similar inhibitory effect on activated C1 (peptide, 5 mg\/kg), or human serum albumin control. Results showed a significant overall increase in tetanic contractile forces of the reperfused EDL in both C1\u2010INH and peptide groups compared to controls. Maximum improvement occurred with peptide treatment at 120\u2010Hz stimulation, with an increase in force from 38 \u00b1 4% of normal in controls to 52 \u00b1 4% in peptide\u2010treated rats. There were no significant differences between C1\u2010INH and peptide groups. Plasma C3 and C4 activities were significantly increased in both treated groups, suggesting inhibition of complement activation. Our results suggest that complement activation is involved in I\/R injury, and inhibition of complement activation may therefore represent a potential therapeutic approach to reducing or preventing I\/R injury. \u00a9 2003 Wiley\u2010Liss, Inc. 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