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.