Role of cytokine hemoadsorption in cardiopulmonary bypass-induced ventricular dysfunction in a porcine model.

Little is known about the effect of cardiopulmonary bypass alone on cardiac function; in an attempt to illuminate this relationship and test a possible mechanism, we used Cytosorb, a device capable of removing virtually all types of circulating cytokines to test the hypothesis that hemoadsorption of cytokines during bypass attenuates bypass-induced acute organ dysfunction. Twelve Yorkshire pigs (50-65 kg) were instrumented with a left ventricular conductance catheter. Baseline mechanics and cytokine expression (tumor necrosis factor [TNF], interleukin-6 [IL-6], and interleukin-10) were measured before and hourly after 1 hour of normothermic cardiopulmonary bypass. Animals underwent bypass without (cardiopulmonary bypass [CPB], n = 6) or with (CPB+HA, n = 6) the CytosorbTM device. Data were compared with "historical" controls (n = 6) that were similarly instrumented but underwent observation instead of bypass. Five hours after separation from bypass (or observation), animals were euthanized. Myocardial water content was determined postmortem. Neither TNF nor IL-6 was significantly elevated in either experimental group versus controls at any time point. Preload recruitable stroke work and dP/dtmax were significantly depressed immediately after separation from bypass in both CPB+HA and CPB and remained depressed for the duration of the experiment. Although Tau remained unchanged, dP/dTmin was significantly diminished in both bypass groups at all time points after separation from bypass. Cytokine hemoadsorption had no effect on any measurable index of function. Differences in postmortem data were not evident between groups. One hour of normothermic CPB results in a significant and sustained decline in left ventricular function that appears unrelated to changes in cytokine expression. Because we did not appreciate a significant change in cytokine concentrations postbypass, the capacity of cytokine hemoadsorption to attenuate CPB-induced ventricular dysfunction could not be assessed.