Prostaglandin E1 reduces myocardial reperfusion injury by inhibiting proinflammatory cytokines production during cardiac surgery.

Abstract

To determine the influence of prostaglandin E1 (PGE1) on the cytokine balance and myocardial protection during cardiac surgery. Prospective, randomized, nonblinded study. University hospital. A total of 19 patients on cardiopulmonary bypass undergoing cardiac surgery. According to randomized sequence, the patients received PGE1 (0.02 approximately 0.05 microg x kg(-1) x min(-1)) from the beginning of surgery to the end of study (PGE1 group, n = 11) or nothing (control group, n = 8). Interleukin (IL)-6, IL-8, IL-10, IL-1 receptor antagonist (IL-1ra), soluble tumor necrosis factor receptor I (sTNF RI), and soluble tumor necrosis factor receptor II (sTNF RII) were measured by enzyme-linked immunosorbent assays. Troponin-T and isoenzyme of creatine kinase with muscle and brain subunits (CK-MB) were measured by enzyme immunoassay and ultraviolet absorption spectrophotometry method, respectively. Serum IL-6 and IL-8 concentrations in both groups increased significantly from 60 mins after declamping the aorta compared with preoperative value (p < .001), However, the increases were greater in the control group than in the PGE1 group (p < .01). Serum IL-10, IL-1ra, sTNF RI, and sTNF RII concentrations increased significantly from 60 mins after declamping the aorta compared with preoperative values in two groups (p < .001, respectively). There were no differences between the two groups. Serum troponin T and CK-MB concentrations increased significantly in the two groups from 60 mins after declamping the aorta (p < .001), but these increases were greater in the control group than in the PGE1 group (p < .01). IL-6 and IL-8 levels correlated with CK-MB concentration (r2 = 0.49, r2 = 0.36; p > .001 respectively). PGE1 suppressed the production of IL-6 and IL-8 but not IL-10, IL-1ra, sTNF RI, or sTNF RII. The change in the balance between pro-and anti-inflammatory cytokines may be one of the most important cytoprotective mechanisms of PGE1.