[Preventive oral rehydration salts III could protect intestinal function in rats with exertional heatstroke]

To observe the damage of various organs of rats with exertional heatstroke (EHS), and to investigate the protective effect of oral rehydration salts III (ORS III) on multi-organ function in rats with EHS.

Fifty-one male Sprague-Dawley (SD) rats were randomly divided into four groups by random digit table: normal control group (n = 13), EHS group (n = 13), EHS+water group (n = 12), and EHS+ORS III group (n = 13). All rats in the EHS groups received adaptive training for 7 days before the experiment. On the 8th day, the rats of EHS+water and EHS+ORS III groups were orally given 20 mL/kg water or ORS III 30 minutes before the experiment. No pretreatment was performed in the EHS group. EHS model was reproduced by forcing rats to run under hot environment. The rats which refused to exercise and which core temperature > 40.5 centigrade were considered as the onset of EHS. The rats in the normal control group were exposed to room temperature (25±2) centigrade and humidity (50±5)% without any treatment. Six hours later, blood of inferior vena cava was collected, and the levels of serum MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH), alanine transaminase (ALT), aspartate transaminase (AST), serum creatinine (SCr), blood urea nitrogen (BUN), serum potassium, serum sodium and serum chloride were determined by automatic chemical analyzer. Serum intestinal fatty acid-binding protein (I-FABP) was determined by enzyme linked immunosorbent assay (ELISA).

The levels of LDH, ALT, AST, BUN, serum sodium and serum chloride in the EHS group were significantly higher than those in the normal control group [LDH (U/L): 1 220±427 vs. 837±485, ALT (U/L): 138 (97, 164) vs. 37 (33, 42), AST (U/L): 409 (380, 566) vs. 86 (78, 104), BUN (mmol/L): 11.7 (9.6, 13.2) vs. 5.9 (5.5, 6.1), serum sodium (mmol/L): 148.0 (143.5, 154.5) vs. 139.0 (138.0, 140.5), serum chloride (mmol/L): 100.9±2.3 vs. 97.3±1.4, all P < 0.05], but no significant difference in CK-MB, SCr or serum potassium could be found [CK-MB (U/L): 1 280±373 vs. 1 379±480, SCr (μmol/L): 38.2±7.5 vs. 35.5±6.3, serum potassium (mmol/L): 5.5 (4.4, 6.2) vs. 4.7 (4.4, 4.9), all P > 0.05]. In the EHS+ORS III group, only serum potassium level was significantly lower than that in the EHS group [mmol/L: 4.0 (3.7, 4.4) vs. 5.5 (4.4, 6.2), P < 0.01], while no significant difference in other parameters was found between the EHS+ORS III group and the EHS group as well as the EHS+water group. Serum I-FABP level in the EHS group was significantly higher than that in the normal control group [μg/L: 36.90 (29.10, 45.00) vs. 11.39 (0.31, 20.80), P < 0.01]. Serum I-FABP level in the EHS+water and EHS+ORS III groups were notably lower than that in the EHS group [μg/L: 24.19 (20.00, 28.36), 0.31 (0.31, 5.58) vs. 36.90 (29.10, 45.00), both P < 0.01], additionally, I-FABP level was much lower in the EHS+ORS III group (P < 0.01).

EHS could lead to liver, intestinal barrier dysfunction and electrolyte disturbance. Pre-treatment of ORS III could alleviate the intestinal dysfunction and electrolyte disorder caused by EHS in rats. It can lower the serum potassium to some extent. However, ORS III failed to protect liver from EHS.