Thermoregulatory, Endocrine, Leukocyte and Hepatic Redox Responses of Wistar Rats (Rattus norvegicus) to Graded Chronic Cyclic Heat Stress

Heat stress (HS) disrupts mammalian homeostasis through interrelated thermoregulatory, endocrine, immune and oxidative pathways, but these pathways are rarely measured together across graded intensities of chronic HS. This study characterized the integrated response of rats to chronic cyclic HS at two intensities. Thirty individually housed male Wistar rats (150 ± 10 g) were randomly assigned to a control group (24 ± 1 °C), mild HS (32 ± 1 °C, 8 h/day) or severe HS (38 ± 1 °C, 8 h/day) for 21 days at 60 ± 5% relative humidity. Relative to the control, final body weight fell by 14.1% and 34.4% under mild and severe HS and feed intake by 15.6% and 42.2%, while the feed conversion ratio increased from 2.65 to 3.04 and 4.33, respectively (P < 0.001). During heating under severe HS, rectal temperature rose from 37.2 to 40.8 °C and respiration rate from 85 to 210 breaths/min. One severe-HS rat reached a humane endpoint on day 18; mortality did not differ among groups (P = 1.000). In samples collected after 15–17 h at 24 °C, severe HS increased the neutrophil/lymphocyte ratio from 0.34 to 3.20 (9.4fold) and serum corticosterone from 45 to 160 ng/mL (3.6-fold). Hepatic malondialdehyde rose from 2.5 to 8.5 nmol/mg protein, whereas superoxide dismutase activity decreased from 55 to 18 U/mg protein (P < 0.001). Chronic cyclic HS at 38 °C therefore exceeds the compensatory capacity of the rat, producing sustained hypothalamic–pituitary–adrenal activation and hepatic redox imbalance at the cost of growth efficiency.