The effects of brain death and 24 hours' storage by hypothermic perfusion on donor heart function in the pig.
The effects on the myocardium of the agonal period and subsequent management have been studied in the pig. Acute ischemia of the brain led to major temporary hemodynamic changes. Brain death, with or without hemodynamic support of the circulation, led to a significant reduction in subsequent myocardial function, associated with some depletion of the myocardial high-energy phosphate and glycogen reserves, although the rate of this depletion was reduced by anaerobic glycolysis. Although 24 hours' storage by continuous hypothermic perfusion of hearts taken from control animals led to only a minimal reduction in myocardial function, storage increased the reduction in function associated with brain death when intravenous fluid and dobutamine support had been given to maintain the brain dead pig in a normotensive state. Storage, however, reduced the anaerobic metabolism seen in hearts functioning in hypotensive brain dead pigs and led to replenishment of the glycogen stores.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001926:Brain Death; D002302:Cardiac Output; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006321:Heart / Q000502:physiology; D006324:Heart Arrest, Induced / Q000379:methods; D006339:Heart Rate; D016027:Heart Transplantation; D007022:Hypotension / Q000503:physiopathology; D007773:Lactates / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D009926:Organ Preservation; D013552:Swine; D013997:Time Factors; D014655:Vascular Resistance
D007773:Lactates; D000255:Adenosine Triphosphate; D006003:Glycogen; D003402:Creatine Kinase