C1-esterase inhibitor in ischemia and reperfusion.
Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte endothelial cell-cell interaction was strikingly reduced in the reperfused tissues as afflection of anti-inflammatory effect.
Horstick
Georg
G
2nd Medical Clinic, Johannes Gutenberg-University Mainz, Germany. horstick@mail.uni-mainz.de
D000818:Animals; D002316:Cardiotonic Agents / Q000378:metabolism / Q000627:therapeutic use*; D003174:Complement C1 Inactivator Proteins / Q000378:metabolism / Q000627:therapeutic use*; D050718:Complement C1 Inhibitor Protein; D003171:Complement Pathway, Classical / Q000502:physiology; D006321:Heart / Q000187:drug effects*; D006801:Humans; D007511:Ischemia / Q000473:pathology; D023421:Models, Animal; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000517:prevention & control
D002316:Cardiotonic Agents; D003174:Complement C1 Inactivator Proteins; D050718:Complement C1 Inhibitor Protein