An in vitro evaluation of prostaglandin El and E2 on hypothermic injury to immature myocytes

The purpose of this study was to evaluate the functional and biochemical effects of Prostaglandin E1 (PGE1) and prostaglandin I2 (PGI2) on cardiac myocytes incubated under hypothermic conditions. Cardiac myocytes were isolated from neonatal rat ventricles and cultured for 4 days with MCDB 107 medium. Following this, 12.5 × 105 myocytes/ flask were incubated at 4°C for 24 h in media with PGE1, at concentrations of 0 M (group E0), 10−9M (group El), 10−8M (group E2), 10−7 M (group E3), or 10−6 M (group E4); or with PGI2 at concentrations of 0 M PGI (group I0), 10−9M (group I1), 10−8M (group I2), 10−7 M (group I3), or 10−6 M (group I4). After hypothermic incubation, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) were measured, and the myocytes were then cultured for 24 h at 37°C to evaluate the recovery of the myocyte beating rate. Of the PGI2 groups, only group 12 recovered significantly more than the control group (group I0), at 47.9 ± 28.5% (mean ± SD) of the control, being the beating rate prior to hypothermic incubation, whereas it was 18.1 ± 9.7% in group I0 (P < 0.025); however, there were no significant differences among the PGE1 groups. Moreover, the release of CPK and LDH was significantly suppressed in groupI2 compared to the control, being 57.7 ± 27.6 mIU/flask (P < 0.05) and 275.1 ±83.0mIU/flask (P < 0.025), respectively, in group 12, and 96.8 ± 38.3 mIU/flask and 439.6 ± 147.1 mIU/flask in group I0. Again, no significant differences were observed among the PGE1 groups. In conclusion, PGI2 was found to have a direct cytoprotective effect on immature myocytes which suggests that PGI2 may promote cardiac preservation in the neonatal period.