6533b831fe1ef96bd1298474
RESEARCH PRODUCT
C1-esterase inhibitor in ischemia and reperfusion.
Georg Horsticksubject
Cardiotonic AgentsImmunologyIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryPharmacologyComplement C1 Inactivator ProteinsProinflammatory cytokineClassical complement pathwayIschemiamedicineImmunology and AllergyAnimalsHumansAnaphylatoxinComplement Pathway ClassicalCardioprotectionbusiness.industryHeartHematologymedicine.diseaseC1 esteraseComplement systemAnesthesiaModels AnimalbusinessPerfusionComplement C1 Inhibitor Proteindescription
Summary 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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2002-10-25 | Immunobiology |