Evidence of functional myocardial ischemia associated with myocardial dysfunction in brain-dead pigs

Background-Cardiac dysfunction after brain death has been documented, but i ts mechanisms remain unclear. Myocardial ischemia has been suggested as a p ossible cause. The aim of the present study was to investigate the existenc e of an imbalance between myocardial oxygen delivery and demand as a possib le cause of myocardial dysfunction in brain-dead pigs. Methods and Results-Interstitial myocardial lactate and adenosine concentra tions were assessed with cardiac microdialysis in 2 groups of animals: brai n-dead pigs (n=7) and brain-dead pigs treated with labetalol (10 +/- 3 mg/k g) (n=7). Heart rate (HR) left ventricular (LV) dP/dt(max), rate-pressure p roduct (RPP), cardiac output (CO), and left anterior descending coronary ar tery blood flow (QLAD) were continuously monitored. Brain-dead pigs exhibit ed a transient significant increase in HR. LV dP/dt(max), RPP, and CO and a limited increase in QLAD. This resulted in functional myocardial ischemia attested to by the significantly increased adenosine and lactate microdialy sate concentrations. In brain-dead pigs treated with labetalol, there was a moderate increase in HR, QLAD, and adenosine microdialysate concentrations ; LV dP/dt(max), RPP, CO, and myocardial lactate concentrations remained st able, confirming the preservation of aerobic metabolism. Conclusions-Brain death was associated with an increase in myocardial inter stitial adenosine and lactate concentrations, as well as with myocardial dy sfunction; all were attenuated by labetatol, suggesting an imbalance betwee n oxygen consumption and oxygen delivery as a possible cause of myocardial dysfunction after brain death.