Original Article

Preservation of Neonatal Myocardial Function Following Ischemic Arrest

Department of Surgery, Division of Thoracic Surgery, SUNY Health Science Center, Syracuse, NY and The Department of Surgery, Division of Thoracic Surgery, University of Michigan, Ann Arbor, MI

^* Address correspondence to: Alfred H. Stammers, BS,CCP, Division of Thoracic Surgery, University of Michigan Hospital, 1500 E. Medical Center Drive, Taubman Health Care Center, 2110 Box 0344, Ann Arbor, MI 48109

Abstract

The protection of the ischemic neonatal myocardium was studied utilizing both cardioplegic and noncardioplegic solutions. Six groups of seven-day-old isolated working rabbit hearts, exposed to 120 minutes of hypothermic (30°C) arrest, were treated with either an oxygenated or nonoxygenated cardioplegic or physiologic saline solution. The results indicated that postischemic aortic flow, stroke volume and cardiac output were significantly depressed in all oxygenated groups, but not in the nonoxygenated cardioplegic groups. Recovery of cardiac output remained near baseline in hearts treated with either single dose (94.4±2.5% mean±SEM) or multidose (94.3±2.3%) nonoxygenated cardioplegia, but was significantly depressed in multidose oxygenated cardioplegia (76.2±6.2%), multidose oxygenated physiological saline (74.8±3.0%), and single dose physiological saline (74.8±3.0%), all at p<05. Coronary sinus creatine kinase was significantly elevated during ischemia in all physiological saline groups as well as the multidose oxygenated cardioplegia group, and remained elevated following reperfusion. In the nonoxygenated cardioplegic groups, creatine kinase was not elevated. This study has demonstrated that the addition of oxygen to either cardioplegic or noncardioplegic physiological saline solutions failed to protect the neonatal myocardium from ischemic or reperfusion related injury.