Controlled cardiac reoxygenation does not improve myocardial function following global myocardial ischemia

It has been shown that abrupt re-exposure of ischemic myocardium to oxygen can lead to increased peroxidative damage to myocytes (oxygen paradox). Controlled cardiac reoxygenation, as an adjunct to substrate-enhanced cardioplegia, has been shown to improve myocardial function and limit reperfusion injury when utilizing standardized hyperoxic cardiopulmonary bypass (CPB). The objective of our study was to evaluate the effect of controlled reoxygenation on myocardial function following global ischemia employing normoxic CPB. Nineteen female swine (30–40 kg) were placed on vented, normoxic CPB. They were subjected to 45–50 min of unprotected global ischemia (aortic cross clamping) followed by 30 min of controlled cardiac reperfusion utilizing substrate-enhanced cardioplegia. Group 1 maintained normoxic pO 2 (O 2 tension of 90–110 mmHg). In Group 2, reoxygenation was titrated gradually and increased from venous to arterial levels (O 2 tensions from 40 to 110 mmHg over 15 min). We measured coronary sinus blood samples for CK, CK-MB, nitric oxide, and conjugated dienes at baseline, 5 min into the cardioplegic resuscitation, 5 min after the cross clamp removal, and just prior to the termination of the study. Hearts were pathologically studied and scored for evidence of tissue peroxidation. Although not significantly different, Group 1 (normoxic reperfusion) animals were more likely to wean from CPB ( p = 0.141) and had a higher mean arterial pressure ( p = 0.556). In Group 1, conjugated dienes were significantly higher 5 min into the resuscitative protocol ( p = 0.018) and at the termination of bypass ( p = 0.035). Five of six animals in Group 1 eventually attained normal sinus rhythm as opposed to three out of 13 in Group 2 ( p = 0.041). There was no significant difference in histology scoring between the two groups for tissue peroxidation. This study of controlled cardiac reoxygenation in a lethal ischemic swine model failed to demonstrate that the use of controlled reoxygenation on the myocardial function following global ischemia was better with maintained normoxic pO 2 (with O 2 tensions of 90–110 mmHg) than when reoxygenation was titrated gradually and increased from venous to arterial levels (O 2 tensions from 40 to 110 mmHg over 15 min).