Premium
C1‐esterase inhibitor and a novel peptide inhibitor improve contractile function in reperfused skeletal muscle
Author(s) -
Toomayan Glen A.,
Chen LongEn,
Jiang HaiXiang,
Qi WenNing,
Seaber Anthony V.,
Frank Michael M.,
Urbaniak James R.
Publication year - 2003
Publication title -
microsurgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 63
eISSN - 1098-2752
pISSN - 0738-1085
DOI - 10.1002/micr.10210
Subject(s) - medicine , peptide , complement system , ischemia , stimulation , endocrinology , skeletal muscle , pharmacology , reperfusion injury , biochemistry , immunology , chemistry , antibody
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. © 2003 Wiley‐Liss, Inc. MICROSURGERY 23:561–567 2003