Acute cardiac inflammatory responses to postischemic reperfusion during cardiopulmonary bypass

Objectives: The investigation centers on whether there is a reperfusion-ind uced specific cardiac inflammatory reaction after bypass surgery. Backgroun d: Cardiopulmonary bypass (CPB) leads to systemic inflammation. Additionall y, cardiac inflammation due to reperfusion could occur. Knowledge about nat ure and time course of this reaction might help to develop cardioprotective interventions. Methods: In 12 patients receiving coronary bypass grafts, a rterial 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 an d IL8 were measured by immunoassay. CD11b, CD41, and CD62 on blood cells we re quantified by flow cytometry. Measurement of CD41, a platelet marker, on neutrophils and monocytes allowed detection of leukocyte-platelet microagg regates. 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 tr anscardially to 95, 88 and 82% of the initial level in the 5th, 10th, and 7 5th min, respectively, suggesting sequestration of activated neutrophils. C D62 on platelets rose about 30% in the 75th min. Initially, leukocyte-plate let microaggregates were formed during coronary passage (+31% of the arteri al level for PMN, +23% for monocytes). During reperfusion, coaggregates wer e 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 reperfusi on after aortic declamping, the coronary bed is already a source of proinfl ammatory stimuli and target for activated leukocytes, partly in conjunction with platelets. Mitigation of these phenomena might help to improve cardia c function after CPB especially in patients at risk. (C) 1999 Elsevier Scie nce B.V. All rights reserved.