[Effects of different core temperatures after heat strike on serum inflammatory cytokines and multiple organ dysfunction syndrome in rats].

OBJECTIVE: To observe the effect of different core temperatures (Tc) after heat strike on serum inflammatory cytokines and multiple organ dysfunction syndrome (MODS) in rat.

METHODS: 120 male Sprague-Dawley (SD) rats were randomly divided into normal control group (n = 30) and heat strike group (n = 90). The rats in heat strike group were put into simulated thermal climate animal module after adaptive training. The module temperature was raised to 39 centigrade in 30 minutes with 65% humidity. The rats ran simultaneously at 15 m/min, on the slope of 0 degree angle, 8 minutes each time, 2 minutes interval, and the heat strike time was 90 minutes. After the rats came out of the module, rectal temperature, which was Tc value, was recorded. The rats died or Tc < 41 centigrade during the experiment were excluded, the remaining 73 rats were divided into three subgroups: 41.0-41.9 centigrade (n = 38), 42.0-42.9 centigrade (n = 26), and ≥43.0 centigrade (n = 9). The rats in the normal control group were reared at temperature of (25±2) centigrade, and humidity of (55±5)%. At 0 hour and 24 hours after the rats came out of the module, femoral artery blood was collected to determine serum interleukins (IL-1α, IL-1β, IL-17), tumor necrosis factor-α(TNF-α) andγ-interferon (IFN-γ) by enzyme-linked immunosorbent assay (ELISA). The cardiac troponin I (cTnI), MB isoenzyme of creatine kinase (CK-MB), serum creatinine (SCr), blood urea nitrogen (BUN), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were determined by automatic biochemical analyzer. The incidence of MODS and the number of accumulative organs within 24 hours of the rats in different Tc of heat strike group were compared and analyzed.

RESULTS: The serum inflammatory cytokines and biochemical parameters at 0 hour after heat strike were significant higher than those of the normal control group, and showed a time dependence. Further analysis showed that the inflammatory response and organ dysfunction in rats were increased gradually with the increase in Tc of rats. Compared with the normal control group, at 24 hours after heat strike, inflammatory cytokines in Tc≥43.0 centigrade rats were increased obviously [IL-1α (ng/L): 13.56±2.07 vs. 2.24±0.62, IL-1β (ng/L): 17.11±1.90 vs. 7.40±1.52, IL-17 (ng/L): 17.00±1.41 vs. 6.00±1.78, TNF-α (ng/L): 16.78±1.79 vs. 7.27±1.74, IFN-γ (ng/L): 21.11±2.09 vs. 10.43±2.31], and the biochemical parameters were also increased obviously [cTnI (ng/L): 50.78±6.67 vs. 20.53±3.09, CK-MB (U/L): 62.89±3.82 vs. 22.00±3.01, SCr (μmol/L): 149.22±4.35 vs. 92.53±8.32, BUN (nmol/L): 55.22±1.99 vs. 19.10±2.02, ALT (U/L): 388.33±4.97 vs. 100.23±10.61, AST (U/L): 361.22±6.53 vs. 97.67±10.54, all P < 0.01]. The incidence of MODS within 24 hours in the heat strike group was 54.79% (40/73), and the higher the Tc, the higher the incidence of MODS, and the more insulted organs [the incidence of MODS in 41.0-41.9 centigrade, 42.0-42.9 centigrade, and ≥43.0 centigrade subgroups was 36.84% (14/38), 65.38% (17/26), 100.00% (9/9), and the organ involvement rate was 12.17% (37/304), 23.08% (48/208), and 48.61% (35/72), respectively, when 8 organs or systems were calculated for each rat, both P < 0.01].

CONCLUSIONS: The higher the Tc of heat strike rats, the stronger the inflammatory reaction and the more serious the damage of tissue, and the more extensive damage of the organs.