Effect of cytokine hemoadsorption on brain death-induced ventricular dysfunction in a porcine model.

OBJECTIVE: In an effort to expand the cardiac donor pool, we tested the hypothesis that hemoadsorption of cytokines attenuates brain death-induced ventricular dysfunction. METHODS: Eighteen Yorkshire pigs (50-60 kg) were instrumented with a left ventricular conductance catheter. Cytokine expression, preload recruitable stroke work, and the diastolic relaxation constant tau were measured at baseline and at hourly intervals for 6 hours after induction of brain death by intracranial balloon inflation (brain death, n = 6) or sham operation (control, n = 6). In a third group (brain death + hemoadsorption, n = 6), 3 hours after induction of brain death, animals were placed on an extracorporeal circuit containing a cytokine-hemoadsorption device for the remaining 3 hours of the experiment. Myocardial water content was measured after the animals were killed. RESULTS: Six hours after induction of brain death, tumor necrosis factor and interleukin-6 were highest in the brain death group (106 ± 13.1 pg/mL and 301 ± 181 pg/mL, respectively), lowest in controls (68.3 ± 8.55 pg/mL and 37.8 ± 11 pg/mL, respectively), and intermediate in the brain death + hemoadsorption group (81.2 ± 35.2 pg/mL and 94.6 ± 20 pg/mL, respectively). Compared with controls, preload recruitable stroke work was significantly reduced in the brain death group 4 hours after the induction of brain death and was 50% of baseline by 5 hours. In the brain death + hemoadsorption group, preload recruitable stroke work was relatively preserved at 80% of baseline at similar time points. Tau remained unchanged in the control and brain death + hemoadsorption groups, whereas in the brain death group it was significantly elevated versus baseline 5 (139.3% ± 21.5%) and 6 (172% ± 16.1%) hours after induction of brain death. Myocardial water content was significantly greater in the brain death group than in the other 2 groups. CONCLUSIONS: Hemoadsorption of cytokines using an extracorporeal circuit attenuates brain death-induced ventricular dysfunction in a porcine model. Improvement in function generally correlates with trends in cytokine expression, but this relationship requires further investigation.