Influence of brain death and cardiac preservation on systolic and diastolic function and coronary circulation in the cross-circulated canine heart

Previous studies have demonstrated hemodynamic instability and cardiac dysf unction in the brain-dead organ donor. It remains unclear if primary cardia c dg dysfunction is responsible for hemodynamic deterioration or decreased cardiac function is secondary to brain death-associated altered loading con ditions. Therefore in the present study the effects of brain death on hemod ynamics and cardiac function were analyzed in vivo in an open chest model a nd ex vivo in a cross-circulated heart preparation. In a second protocol, t he impact of brain death-associated hemodynamic changes on postischemic gra ft function was investigated. Brain death was induced injecting saline in a subdural Foley catheter. Induction of brain death led to a hyperdynamic re action followed by hemodynamic deterioration with a decrease of systemic va scular resistance and myocardial contractility. If the hearts were explante d and assessed ex vivo, no differences were found between control and brain -dead hearts. Furthermore, both control and brain-dead hearts showed full f unctional recovery after 4 hours of hypothermic ischemic storage. Despite h emodynamic deterioration in situ after brain death, there were no differenc es between the postischemic function of control and brain-dead hearts. Thes e results indicate that myocardial dysfunction is not irreversible and may be secondary to altered loading conditions, and that the recovery of cardia c function after long-term hypothermic storage is not impaired by the hemod ynamic changes observed in situ after brain death induction. These data may also indicate that potential donor hearts might not be excluded from trans plantation on the basis of impaired hemodynamic characteristics, especially if they are evaluated by load-dependent parameters.