title: Acute cardiac inflammatory responses to postischemic reperfusion during cardiopulmonary bypass.
abstract: OBJECTIVE
  The investigation centers on whether there is a reperfusion-induced specific cardiac inflammatory reaction after bypass surgery.
  
  
  BACKGROUND
  Cardiopulmonary bypass (CPB) leads to systemic inflammation. Additionally, cardiac inflammation due to reperfusion could occur. Knowledge about nature and time course of this reaction might help to develop cardioprotective interventions.
  
  
  METHODS
  In 12 patients receiving coronary bypass grafts, arterial and coronary venous blood was obtained before onset of CPB, and 1, 5, 10, 25, 35 and 75 min after cardiac reperfusion. Plasma levels of IL6 and IL8 were measured by immunoassay. CD11b, CD41, and CD62 on blood cells were quantified by flow cytometry. Measurement of CD41, a platelet marker, on neutrophils and monocytes allowed detection of leukocyte-platelet microaggregates.
  
  
  RESULTS
  Transcardiac veno-arterial difference of IL6 rose in the 10th and 25th min of reperfusion (from 0 to 7 pg/ml; p < 0.05), and after 75 min (15 pg/ml). IL8 did not change. CD11b on neutrophils (PMN) decreased transcardially to 95, 88 and 82% of the initial level in the 5th, 10th, and 75th min, respectively, suggesting sequestration of activated neutrophils. CD62 on platelets rose about 30% in the 75th min. Initially, leukocyte-platelet microaggregates were formed during coronary passage (+31% of the arterial level for PMN, +23% for monocytes). During reperfusion, coaggregates were retained (PMN: -1% and -7% in the 5th and 10th min, monocytes: -22%, -13% and -12% in the 1st, 5th and 10th min.
  
  
  CONCLUSIONS
  During early reperfusion after aortic declamping, the coronary bed is already a source of proinflammatory stimuli and target for activated leukocytes, partly in conjunction with platelets. Mitigation of these phenomena might help to improve cardiac function after CPB especially in patients at risk.
authors.affiliation: Department of Physiology, University of Munich, Germany. s.zahler@lrz.uni-muenchen.de
authors.forename: S
authors.initials: S
authors.lastname: Zahler
authors.forename: P
authors.initials: P
authors.lastname: Massoudy
authors.forename: H
authors.initials: H
authors.lastname: Hartl
authors.forename: C
authors.initials: C
authors.lastname: Hähnel
authors.forename: H
authors.initials: H
authors.lastname: Meisner
authors.forename: B F
authors.initials: BF
authors.lastname: Becker
mesh_terms: D000704:Analysis of Variance; D001792:Blood Platelets / Q000276:immunology; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D002448:Cell Adhesion; D005260:Female; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000032:analysis*; D016177:Macrophage-1 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D015428:Myocardial Reperfusion Injury / Q000276:immunology*; D009206:Myocardium / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D015539:Platelet Activation; D019087:Selectins / Q000032:analysis; D013997:Time Factors
chemical_list: D015850:Interleukin-6; D016177:Macrophage-1 Antigen; D019087:Selectins