Cardiovascular and thermoregulatory dysregulation over 24 h following acute heat stress in rats

The influences of severe heat stroke (HS) on cardiovascular function during recovery are incompletely understood. We hypothesized that HS would elicit a heart rate (HR) increase persisting through 24 h of recovery due to hemodynamic, thermoregulatory, and inflammatory events, necessitating tachycardia to support mean arterial pressure (MAP). Core temperature (T-c), HR, and MAP were measured via radiotelemetry in conscious male Fischer 344 rats (n = 22; 282.4 +/- 3.5 g) during exposure to 37 degrees C ambient temperature until a maximum T-c of 42.0 degrees C, and during recovery at 20 degrees C ambient temperature through 24 h. Rats were divided into Mild, Moderate, and Severe groups based on pathophysiology. HS rats exhibited hysteresis relative to T-c with HR higher for a given T-c during recovery compared with heating (P < 0.0001). "Reverse" hysteresis occurred in MAP with pressure during cooling lower than heating per degree T-c (P < 0.0001). Mild HS rats showed tachycardia [P < 0.01 vs. control (Con)] through 8 h of recovery, elevated MAP (P < 0.05 vs. Con) for the initial 5 h of recovery, with sustained hyperthermia (P < 0.05 vs. Con) through 24 h. Moderate HS rats showed significant tachycardia (P < 0.01 vs. Con), normal MAP (P > 0.05 vs. Con), and rebound hyperthermia from 4 to 24 h post-HS (P < 0.05 vs. Con). Severe HS rats showed tachycardia (P < 0.05 vs. Con), hypotension (P < 0.01 vs. Con), and hypothermia for 24 h (P < 0.05 vs. Con). Severe HS rats showed 14-and 12-fold increase in heart and liver inducible nitric oxide synthase expression, respectively. Hypotension and hypothermia in Severe HS rats was consistent with inducible nitric oxide synthase-mediated systemic vasodilation. These findings provide mechanistic insight into hemodynamic and thermoregulatory impairments during 24 h of HS recovery.