Effects of Thyrotropin Releasing Hormone on the Developing Rat Heart

Olsen et al, reported that changes simulating hypertrophic cardiomyopathy were produced in newborn rats when triiodothyroacetic acid (triac, an analogue of thyroxine) was given during the fetal period. However, triac is barely transported across the rat placenta, while thyrotropin releasing hormone (TRH) is readily transported across the rat placenta and acts directly on the fetus. In this study, TRH was administered to pregnant female rats and its effects on the hearts of their offspring were studied using morphologic and immunohistochemical techniques with Bromodeoxyuridine (BrdU). The hearts of the TRH-treated newborn rats showed disproportionate septal hypertrophy and frequent septal myocardial fiber disarray. The labeling index of BrdU in the septum was significantly higher in the TRH-treated newborn rats than in controls. In the TRH-treated newborn rats, the labeling index of BrdU was significantly higher in the septum than in the free wall. These results indicate that TRH administration during the fetal period causes an increase in myocardial cellular proliferation, especially in the septum, resulting in disproportionate septal hypertrophy in the newborn rats.