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Leucocytes and cardiopulmonary bypass: in vitro production of oxygen free radicals and trapping in the reperfused myocardium

Departments of Physiology and Surgery. University of Tromsø, Norway

J. Vaage

Departments of Physiology and Surgery. University of Tromsø, Norway

M. Lie

Departments of Physiology and Surgery. University of Tromsø, Norway

D. Sørlie

Departments of Physiology and Surgery. University of Tromsø, Norway

OD Mjøs

Departments of Physiology and Surgery. University of Tromsø, Norway

The production of oxygen free radicals (OFR) by leucocytes was evaluated ex vivo by chemiluminescence (CL) before, during and after routine coronary artery bypass surgery (group A, n=11). The possibility of leucocyte trapping in the coronary circulation during the early reperfusion period was also investigated (group B, n=9). In group A, arterial blood samples were taken immediately before the start of surgery during anaesthesia, five minutes before and five and 30 minutes after the start of cardiopulmonary bypass (CPB), five minutes before and five and 30 minutes after the start of reperfusion of the heart, and then four and 24 hours after the end of CPB. In group B, arterial and coronary sinus blood samples were simultaneously drawn five and 30 minutes after the release of the aortic crossclamp. All blood samples were corrected for haemodilution. In group A, both CL and the level of circulating leucocytes declined during CPB. The lowest value of CL was measured 30 minutes after the start of CPB (69± 2% of baseline values) (mean±SEM). The lowest level of leucocytes was found after 30 minutes of CPB: 2.6±0.4 (10⁹/l) vs 4.2±0.5 before surgery. Twenty-four hours after CPB, CL was increased to 170±49% and a leucocytosis was present (12.2±1.1). In group B, after five minutes of reperfusion the number of circulating leucocytes in arterial blood was 3.8±0.9 x 10 ⁹/l as compared to 2.2±0.5 x 10⁹/l in the coronary sinus (p<0.0017). However, no such difference was found after 30 minutes of reperfusion. The decreased CL during CPB was probably due to in vivo activation and exhaustion of leucocytes. The postischaemic trapping of these cells may play a pathogenetic role in reperfusion injury.

Perfusion, Vol. 5, No. 3, 169-180 (1990)
DOI: 10.1177/026765919000500303


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