title: Soluble complement receptor type I limits damage during revascularization of ischemic myocardium.
abstract: BACKGROUND
  This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium.
  
  
  METHODS
  In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4=normal to -1=dyskinesia), and infarct size (area of necrosis versus area at risk).
  
  
  RESULTS
  After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1%+/-0.09% versus 7.8%+/-0.04%, respectively; p < 0.002), less myocardial acidosis (-0.41+/-0.03 versus -0.72+/-0.03, respectively; p < 0.0001), higher wall motion scores (3.1+/-0.09 versus 1.67+/-0.16, respectively; p < 0.0001), and smaller infarct size (24.6%+/-2.0% versus 41%+/-1.3%, respectively; p < 0.0001).
  
  
  CONCLUSIONS
  Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.
authors.affiliation: Department of Cardiothoracic Surgery, Boston Medical Center, Massachusetts 02118, USA.
authors.forename: H L
authors.initials: HL
authors.lastname: Lazar
authors.forename: T
authors.initials: T
authors.lastname: Hamasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Bao
authors.forename: S
authors.initials: S
authors.lastname: Rivers
authors.forename: S A
authors.initials: SA
authors.lastname: Bernard
authors.forename: R J
authors.initials: RJ
authors.lastname: Shemin
mesh_terms: D000138:Acidosis / Q000209:etiology / Q000503:physiopathology; D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology / Q000503:physiopathology; D003167:Complement Activation / Q000187:drug effects; D003169:Complement Inactivator Proteins / Q000008:administration & dosage / Q000627:therapeutic use*; D003327:Coronary Disease / Q000503:physiopathology; D006324:Heart Arrest, Induced; D006461:Hemolysis; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007262:Infusions, Intravenous; D009200:Myocardial Contraction / Q000187:drug effects; D017202:Myocardial Ischemia / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D011897:Random Allocation; D011951:Receptors, Complement / Q000008:administration & dosage / Q000627:therapeutic use*; D013552:Swine
chemical_list: D003169:Complement Inactivator Proteins; D011951:Receptors, Complement