Effect of temperature on isoproterenol-induced increases in left ventricular developed pressure

The goal of this project was to determine the effects of elevated cardiac temperature on preload-dependent and preload-independent regulation of left ventricular developed pressure (LVDP) in Langendorff-perfused, electrically paced (420bpm), Sprague-Dawley rat hearts. LVDP responses to steady-state isoproterenol infusions (10−8M) were determined at 37, 38, 39, and 40°C. Preload-dependent LVDP was determined at 37 and 40°C. Isoproterenol-induced LVDP and preload-dependent LVDP time controls were conducted in a separate group maintained at 37°C. The percent increase in LVDP during isoproterenol infusion significantly decreased at 40°C to 42±6 (SE), compared to 55±9, 55±6, and 53±7% at 37, 38, and 39°C, respectively. No significant differences were observed in the percent increase in LVDP to isoproterenol among the corresponding time controls (50±6, 47±3, 56±4, and 56±5%). Preload-dependent LVDP decreased across the experimental protocol, but there were no cardiac temperature effects. These data indicate that β-adrenergic mediated contractility is not altered by moderate heating from normothermia but is compromised at very high temperatures (40°C). Cardiac temperatures from 37 to 40°C do not alter the inherent preload-dependent LVDP, indicating that the Frank–Starling relation is not directly affected within this temperature range. •Does left-ventricular temperature alter preload-independent & -dependent developed pressure?•The isoproterenol-induced increase in developed pressure decreased at 40°C vs. 37, 38, and 39°C.•Thus, β-adrenergic contractility is not altered by moderate heating but is at high temperatures.•Left-ventricular temperature from 37 to 40°C did not alter preload-dependent developed pressure.•Thus, Frank–Starling relations are not directly affected within this temperature range.