Korean J Physiol Pharmacol.  1999 Dec;3(6):579-586.

Effect of C1 esterase inhibitor on the cardiac dysfunction following ischemia and reperfusion in the isolated perfused rat heart

• Lee GY
• Shin YK
• Jang YY
• Song JH
• Kim DJ

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.

Keyword

Ischemia/Reperfusion; Rat heart; PMNs; Complement esterase inhibitor (C1 INH)

MeSH Terms

Animals
Complement C1 Inhibitor Protein*
Complement C1s*
Heart*
Ischemia*
Myocardial Ischemia
Myocardium
Neutrophil Activation
Neutrophils
Perfusion
Peroxidase
Plasma
Rats*
Reperfusion Injury
Reperfusion*
Complement C1 Inhibitor Protein
Complement C1s
Peroxidase