The purpose of this study is to determine whether aspirin can reduce interleukin-1beta(IL-1beta) concentration and exert protective effects against heatstroke. The heatstroke rat model was established through exposing rat to a high ambient temperature (HAT, Ta 41 degrees C, relative humidity 65%) in a simulative HAT chamber to induce heatstroke. Three parts were performed in the present experiment: (1) To determine the effects of pretreatment with aspirin against heatstroke;(2) To prove the effects of specifically reducing inducible nitric oxide synthase (iNOS) against rat heatstroke by iNOS selective prohibitor aminoguanidine (AG);(3) To determine the effects of aspirin against heatstroke and fatigue. In part 1 and 2, Sprague-Dawley rats were randomly assigned to control and aspirin groups or AG groups respectively. Mean arterial blood pressure (MAP), colonic temperature (T(co)), electrocardiograph (ECG) were monitored during heat exposure (HE) and blood samples were taken 0 and 60 min after HE for IL-1betaassay or nitric oxide (NO) assay. In part 3, additional control and aspirin groups of conscious rats were put in a barrel with 41 degrees C water and kept swimming until drowning over 10 s, and then intervals were recorded as survival time. The results from part 1 showed that from 0 to 50 min after HE, MAPs of control group and aspirin group were not significantly different. About 50-60 min after HE, MAPs of both groups were decreased abruptly and MAPs of control group were decreased significantly in comparison with those of aspirin group. T(co) of both groups was increased until to 42 degrees C, without significant difference. Time of heatstroke onset was not significantly different, while survival time was significantly longer in aspirin group than that in control group. Plasma IL-1betaconcentrations in both groups were significantly increased after HE, and the concentration was significantly higher in the control group than that in aspirin group 60 min after HE. In part 3, the survival time was significantly longer in aspirin group than that in control group. In part 2, MAPs of both groups from 0 to 50 min after HE were not significantly different, whereas 55-60 min after HE, MAPs of control group were decreased significantly in comparison with those of AG group;T(co) of both groups was increased after HE until to 42 degrees C, but without significant difference. The time of the heatstroke onset and survival time of AG group were significantly longer than that of control group;the plasma NO concentrations of two groups were significantly higher 60 min after HE than those 0 min after HE, and the plasma NO concentration of control group was significantly higher than that of AG group 60 min after HE. In conclusion, IL-1betamay contribute to heatstroke through inducing iNOS, which attenuates the tone of peripheral blood vessel, and pretreatment with aspirin can provide preventive effects against heatstroke and reinforce the heat and fatigue endurance, which may be associated with inhibition of systemic IL-1betalevels and local iNOS levels.