Environment-induced heat stress causes ventricular-dependent biochemical changes in the heart in female pigs.

Abstract

Prolonged exposure to inescapable heat and humidity can lead to environment-induced heat stress (EIHS). The extent to which EIHS damages the heart is largely unknown, though our previous work indicated EIHS caused ventricle-dependent changes. The purpose of this investigation was to determine the extent to which EIHS increased proteolysis and altered calcium homeostasis in the left (LV) and right ventricles (RV). We hypothesized that in the RV, EIHS would increase proteolysis, whereas in the LV, EIHS would cause calcium dysregulation. To test this hypothesis, 3-month-old female pigs were assigned to thermoneutral (TN; 20 ± 0.2°C; n = 8) or EIHS (37.4 ± 0.2°C; n = 8) conditions for 24 h and hearts were removed. In the RV, we discovered increased markers of proteolysis such that the relative protein abundance of calpain II, MuRF-1, and MAFbx/Atrogin1 was increased, as was a marker of calpain activity. Conversely, in the LV, we discovered that EIHS increased the relative protein abundance of calcium regulatory proteins, including PMCA, SERCA2a, STIM1, calsequestrin, CaMKII, and VDAC. These data demonstrate EIHS caused ventricular-dependent changes such that in the RV, the balance of proteostasis was shifted toward proteolysis and in the LV, calcium dysregulation may underlie, at least in part, our previous discovery of ventricular thickening.