Effect of C1 esterase inhibitor on the cardiac dysfunction following ischemia and reperfusion in the isolated perfused rat heart.
- Author:
Geon Young LEE
1
;
Yong Kyoo SHIN
;
Yoon Young JANG
;
Jin Ho SONG
;
Dae Joong KIM
Author Information
1. Department of Pharmacology, College of Medicine, Chung-Ang University, 221 Heuk-Suk Dong, Dong-Jak Ku, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Ischemia/Reperfusion;
Rat heart;
PMNs;
Complement esterase inhibitor (C1 INH)
- MeSH:
Animals;
Complement C1 Inhibitor Protein*;
Complement C1s*;
Heart*;
Ischemia*;
Myocardial Ischemia;
Myocardium;
Neutrophil Activation;
Neutrophils;
Perfusion;
Peroxidase;
Plasma;
Rats*;
Reperfusion Injury;
Reperfusion*
- From:The Korean Journal of Physiology and Pharmacology
1999;3(6):579-586
- CountryRepublic of Korea
- Language:English
-
Abstract:
Complement-mediated neutrophil activation has been hypothesized to be an important mechanism of reperfusion injury. It has been proposed that C1 esterase inhibitor (C1 INH) may prevent the complement-dependent activation of polymorphonuclear leukocytes (PMNs) that occurs within postischemic myocardium. Therefore, The effect of C1 INH was examined in neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of C1 INH (5 mg/Kg) to I/R hearts in the presence of PMNs (100 X 106) and homologous plasma improved coronary flow and preserved cardiac contractile function (p<0.001) in comparison to those I/R hearts receiving only vehicle. In addition, C1 INH significantly (p<0.001) reduced PMN accumulation in the ischemic myocardium as evidenced by an attenuation in myeloperoxidase activity. These findings demonstrate the C1 INH is a potent and effective cardioprotective agent inhibits leukocyte-endothelial interaction and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.
