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

Objective: To determine the influence of prostaglandin E-1 (PGE,) on the cytokine balance and myocardial protection during cardiac surgery. Design: Prospective, randomized, nonblinded study. Setting University hospital. Patients: A total of 19 patients on cardiopulmonary bypass undergoing cardiac surgery. Interventions: According to randomized sequence, the patients received PGE(1) (0.02 similar to 0.05 mu g.kg(-1) min(-1)) from the beginning of surgery to the end of study (PGE, group, n = 11) or nothing (control group, n = 8). Measurements and Main Results: Interleukin (IL)-6, IL-8, IL-10, IL-l 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 PGE(1) 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 PGE, group (P < .01). IL-6 and IL-8 levels correlated with CK-MB concentration (r(2) = 0.49, r(2) = 0.36; p > .001 respectively). Conclusions: PGE(1) 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 PGE,.