Interleukin-1-induced myocardial depression in an isolated beating heart preparation.

Myocyte necrosis and interstitial edema seen with severe cardiac allograft rejection are probable major contributors to associated cardiac dysfunction. The monokine interleukin-1 (IL-1), although important in recruitment of the immunologic response, stimulates release of a variety of vasoactive compounds, including prostaglandin E2. In addition, IL-1 has been shown to alter protein metabolism in both skeletal and cardiac atrial muscle. IL-1 was infused into the aortas of isolated perfused rat hearts to test the hypothesis that it might directly induce myocardial dysfunction. Heart rate, generated force, creatine phosphokinase release, and lactate production were measured serially. Compared with the control group, there was a significant reduction of force (expressed as percentage of baseline) in the IL-1--treated group (for example 87% +/- 7% versus 77% +/- 11% at 60 minutes, p = 0.016; 65% +/- 11% versus 50% +/- 14% at 180 minutes, p = 0.018). IL-1--treated and control groups did not differ in heart rates, lactate production, or creatine phosphokinase release. In this model, IL-1 produces a depression in myocardial force that does not appear to be due to myocardial cell necrosis or to a change from aerobic to anerobic metabolism.