The purpose of this study was to examine the effect of heat stress on diaphragm function in rat with pulmonary hypertension (PH). Male Wistar rats were randomly assigned to control (C), control with heat stress (C+H), monocrotaline-induced PH (M), monocrotalineinduced PH with heat stress (M+H) group. PH was induced in rats by a single injection of monocrotaline (60 mg/kg). C+H and M+H group were exposed to heated water at 42 degree for 30 min every other day for 4 weeks. After 4 weeks of injection, diaphragm muscle was removed and analyzed for force production. To assess mechanisms underlying the effects of heat stress, we measured expression of myofibrillar proteins, heat shock proteins (HSP), antioxidative enzymes, and redox modifications. Compared with C group, there was a decreased tetanic force per cross-sectional area in the M group. The levels of HSP72 were increased in the CH and MH groups, but there was no difference in the expression levels of myosin and troponin T between the groups. The levels of superoxide dismutase (SOD) 2 and catalase were increased in M+H group. The levels of redox modification, including 3-nitrotyrosin, malondialdehyde, S-Nitroso-Cysteine, and methionine sulfoxide, did not differ between the groups. The present study suggests that heat stress can ameliorate PH-induced diaphragm dysfunction. These protective effects could result from increased antioxidative capacities through upregulation of SOD2 and catalase.
