| Heatstroke (HS) is a medical emergency caused by prolonged exposure to high ambient temperature (HAT) and characterized by hypotension, delirium, coma and convulsion. Despite adequate lowering of body temperature and aggressive treatment, HS is always associated with high mortality rates of 12-21%. In the south of China, where the summers always last a long time with a characteristic of high temperature and high humid climate, and HS and deaths associated with HS have attacked more frequently in recent years. The incidence of such deaths may increase with global wanning and the predicted worldwide increase frequency and intensity of heat waves. It was once believed that the main cause of death in HS is related to the damage of central nervous system (CNS) after prolonged exposure to HAT. However, evidence has accumulated indicates that the cause of death is probably not CNS damage, but systemic hemodynamic deterioration .Some people consider that endothelial dysfunction caused by HAT and consequent increased concentration of endotoxin is the fatal factor of decreased vasoconstrictor tone and profound hypotension, and IL-1β is involved in this complex process. A recent study suggested that pretreatment with aspirin can provide the preventive effects against inflammation-induced endothelial dysfunction which may be through modulation of cytokine (such as IL-1β) cascade. We speculate that pretreatment with aspirin may attenuate the increase of the plasma levels of IL-1β and inhibit IL-1β-stimulated iNOS and NO production in rats with HS, consequently may provide protective effects on rats with HS.1. Effects of selective iNOS prohibitor aminoguanidine on rat HS: Methods The rats were randomly assigned into 1 of the following 2 groups: control group or aminoguanidine (AG) group. The rats of control group(n=10) and AG group (n=10) were exposed to a HAT ( Ta 41C, relative humidity 65%) to induce HS, arterial blood pressures, colonic temperature (Tco), electrocardiograph (ECG) were monitored. The other rats of both groups (both n=10) were exposed to a HAT (41C, relative humidity 65%), and the blood samples were taken at 0, 60min after heat exposure (HE) for determination of the plasma NO concentrations. Results (1) From 0 min to 50min after HE, MAPs of two groups were not significantly different, but at about 55min-60min after HE, MAPs of control group were decreased significantly differently from that of AG group, K value and dicrotic pulse relative height (hD/H) were gradually decreased after HE, especially at 40 min after HE, K value of control group decreased significantly comparison with that of AG group;(2) Heart rate (HR) and QT interval of both groups were increased after HE ,while PR interval were decreased;(3) Tco of both groups were increased after HE until Tco increased to 42 C (the onset of HS), but there was not significantly difference between the two groups; (4) The time of the onset of heatstroke (TOHS) and survival time(ST) of AG group were significantly longer than that of control group; (5) the plasma NO concentrations of the two groups were significantly higher at 60min after HE than at 0min after HE, and the plasma NO concentrations of control group were significantly higher than that of AG group at 60 min after HE.2. Pretreatment with aspirin reduces IL-1β concentration and provides protective effects against rat heatstroke: Methods The rats were randomly assigned into control group and ASA group, the rats of control group were treated with 0.5%CMC, and the rats of ASA group were treated with 0.5%CMC+ 0.25% ASA at 12h before the HE. (l)The rats of the two groups (both n=10) were exposed to a HAT (Ta 41C,relative humidity 65%) to induce HS, arterial blood pressures, Tco, ECG were monitored;(2)The other rats of both groups (n=7) were exposed to a HAT (Ta 41 C,relative humidity 65%),and the blood samples were taken at 0, 60min after HE for determining the plasma IL-1β concentrations of the two groups;(3)To evaluate the effectof pretreatment with aspirin on the anti-fatigue an...
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