Abstract |
To determine the role of inhibition of complement activation in the contractile function of skeletal muscle ischemia-reperfusion (I/R) injury, the rat extensor digitorum longus (EDL) muscles underwent 3 h ischemia and received human C1-esterase inhibitor (C1-INH, 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-INH and peptide groups compared to controls. Maximum improvement occurred with peptide treatment at 120-Hz stimulation, with an increase in force from 38 +/- 4% of normal in controls to 52 +/- 4% in peptide-treated rats. There were no significant differences between C1-INH 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.
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Authors | Glen A Toomayan, Long-En Chen, Hai-Xiang Jiang, Wen-Ning Qi, Anthony V Seaber, Michael M Frank, James R Urbaniak |
Journal | Microsurgery
(Microsurgery)
Vol. 23
Issue 6
Pg. 561-7
( 2003)
ISSN: 0738-1085 [Print] United States |
PMID | 14705072
(Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Copyright | Copyright 2003 Wiley-Liss, Inc. |
Chemical References |
- Complement C1 Inactivator Proteins
- Complement C1q
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Topics |
- Animals
- Complement Activation
- Complement C1 Inactivator Proteins
(pharmacology)
- Complement C1q
(pharmacology)
- Disease Models, Animal
- Female
- Humans
- Muscle Contraction
(drug effects, physiology)
- Muscle, Skeletal
(drug effects, physiology)
- Probability
- Rats
- Rats, Sprague-Dawley
- Reference Values
- Reperfusion Injury
(drug therapy, pathology)
- Sensitivity and Specificity
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