Cardiovascular Dysregulation during Heat Stroke Recovery in Rats

We showed previously that cardiovascular adjustments during uncompensable heat stress (HS) provide insight into the severity of pathophysiological responses in rats. The present analysis evaluated the association between hemodynamic and thermoregulatory patterns and morbidity and pathophysiology during 24h of HS recovery. Conscious male F344 rats (N=22), radiotelemetered for continuous HR, BP and core temperature (T c ) measurements, were monitored during exposure to ambient temperature (T a ) of 37 ° C to T cMax of 41.9 ± 0.1 ° C and during 24h of recovery at T a of 20°C. Control (CON) rats were maintained at T a of 20°C during experimentation. Rats with MILD and MODERATE HS responses demonstrated sustained tachycardia ( p <0.01 vs CON), normal BP ( p =0.995 vs CON), and hyperthermia ~1°C above CON values ( p < 0.01) during recovery. Rats with SEVERE responses developed hypothermia ~1°C below CON values ( p< 0.01) and hypotension ~20mmHg below CON ( p <0.01) during recovery. The SEVERE group demonstrated a ~51‐fold increase in cardiac IL‐6 gene expression at 24h ( p <0.01), suggesting an inflammatory response that was substantially greater than that observed in MODERATE animals (7‐fold; p <0.05); MILD were not different from CON ( p< 0.35). At 24h, cardiac gene expression of inducible nitric oxide synthase (iNOS) was elevated 14‐fold in the SEVERE group. The increase in iNOS could contribute to the hypotension and hypothermia via promotion of peripheral vasodilation. These findings extend our understanding of HS‐induced cardiovascular dysregulation and provide mechanistic insight into pathophysiology contributing to multi‐organ failure in HS patients. Funded by USAMRMC; author views not official US Army or DOD policy