Heat shock protein expression protects against cerebral ischemia and monoamine overload in rat heatstroke.
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This study attempted to ascertain whether the ischemic damage to neurons and monoamine overload in brain that occur during rat heatstroke can be attenuated by heat shock protein (HSP) 72 induction. Effects of heatstroke on mean arterial pressure (MAP), cerebral blood flow (CBF), brain dopamine (DA) and serotonin (5-HT) release, and neural damage score were assayed in rats 0, 16, or 48 h after heat shock (42 degrees C for 15 min) or chemical stress (5 mg/kg sodium arsenite ip). Brain HSP 72 in rats after heat shock or chemical stress was detected by Western blot, and brain monoamine was determined by a microdialysis probe combined with high-performance liquid chromatography. Heatstroke was induced by exposing the animal to a high ambient temperature (43 degrees C); the moment at which MAP and CBF decreased from their peak values was taken as the time of heatstroke onset. Prior heat shock or chemical stress conferred significant protection against heatstroke-induced hyperthermia, arterial hypotension, cerebral ischemia, cerebral DA and 5-HT overload, and neural damage and correlated with expression of HSP 72 in brain at 16 h. However, at 48 h, when HSP 72 expression returned to basal values, the above responses that occurred during the onset of heatstroke were indistinguishable between the two groups (0 h vs. 48 h). These results lead to the hypothesis that the brain can be preconditioned by thermal or chemical injury, that this preconditioning will induce HSP 72, and that HSP 72 induction will correlate quite well with anatomic, histochemical, and hemodynamic protection in rat heatstroke. (+info)
Disseminated zygomycosis due to Rhizopus schipperae after heatstroke.
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A 21-year-old woman suffered heatstroke and developed diarrhea while trekking across south Texas. The heatstroke was complicated by seizures, rhabdomyolysis, pneumonia, renal failure, and disseminated intravascular coagulation. The patient's stool and blood cultures grew Campylobacter jejuni. The patient subsequently developed paranasal and gastrointestinal zygomycosis and required surgical debridement and a prolonged course of amphotericin B. The zygomycete cultured was Rhizopus schipperae. This is only the second isolate of R. schipperae that has been described. R. schipperae is characterized by the production of clusters of up to 10 sporangiophores arising from simple but well-developed rhizoids. These asexual reproductive propagules are produced on Czapek Dox agar but are absent on routine mycology media, where only chlamydospores are observed. Despite multiorgan failure, bacteremia, and disseminated zygomycosis, the patient survived and had a good neurological outcome. Heatstroke has not been previously described as a risk factor for the development of disseminated zygomycosis. (+info)
Temperature and air pollution as risk factors for heat stroke in Tokyo, July and August 1980-1995.
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Heat stroke is associated with prolonged exposures to high air temperatures that usually occur in the summer months of July and August in Tokyo, Japan. Also during July and August, residents of Tokyo are often exposed simultaneously to high concentrations of air pollutants. To assess the impacts of these combined exposures, daily numbers of heat stroke emergency transport cases/million residents for Tokyo were stratified by gender and three groups: 0-14, 15-64; and > 65 years of age, for the months of July and August in 1980-1995. A regression model was constructed using daily maximum temperature (Tmax) and daily average concentrations of NO2 and O3 as model covariates. Classification indices were added to make it possible to compare the expected number of heat stroke cases by age and gender. Lag times of 1-4 days in Tmax and air quality covariates and terms to account for interactions between pairs of model covariates were also included as additional risk factors. Generalized linear models (GLMs), assuming a Poisson error structure for heat stroke emergency transport cases, were used to determine which covariates were significant risk factors for heat stroke for the three age groups of males and females. Same-day Tmax and concentrations of NO2 were the most significant risk factors for heat stroke in all age groups of males and females. The number of heat stroke emergency transport cases/million residents was greater in males than in females in the same age groups. The smallest number of heat stroke emergency transport cases/million residents occurred for females 0-14 years of age and the greatest number of heat stroke emergency transport cases/million residents occurred for males > 65 years of age. (+info)
Heat exhaustion in a deep underground metalliferous mine.
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OBJECTIVES: To examine the incidence, clinical state, personal risk factors, haematology, and biochemistry of heat exhaustion occurring at a deep underground metalliferous mine. To describe the underground thermal conditions associated with the occurrence of heat exhaustion. METHODS: A 1 year prospective case series of acute heat exhaustion was undertaken. A history was obtained with a structured questionnaire. Pulse rate, blood pressure, tympanic temperature, and specific gravity of urine were measured before treatment. Venous blood was analysed for haematological and biochemical variables, during the acute presentation and after recovery. Body mass index (BMI) and maximum O2 consumption (VO2 max) were measured after recovery. Psychrometric wet bulb temperature, dry bulb temperature, and air velocity were measured at the underground sites where heat exhaustion had occurred. Air cooling power and psychrometric wet bulb globe temperature were derived from these data. RESULTS: 106 Cases were studied. The incidence of heat exhaustion during the year was 43.0 cases/million man-hours. In February it was 147 cases/million man-hours. The incidence rate ratio for mines operating below 1200 m compared with those operating above 1200 m was 3.17. Mean estimated fluid intake was 0.64 l/h (SD 0.29, range 0.08-1.50). The following data were increased in acute presentation compared with recovery (p value, % of acute cases above the normal clinical range): neutrophils (p < 0.001, 36%), anion gap (p < 0.001, 63%), urea (p < 0.001, 21%), creatinine (p < 0.001, 30%), glucose (p < 0.001, 15%), serum osmolality (p = 0.030, 71%), creatine kinase (p = 0.002, 45%), aspartate transaminase (p < 0.001, 14%), lactate dehydrogenase (p < 0.001, 9.5%), and ferritin (p < 0.001, 26%). The following data were depressed in acute presentation compared with recovery (p value, % of acute cases below the normal clinical range): eosinophils (p = 0.003, 38%) and bicarbonate (p = 0.011, 32%). Urea and creatinine were significantly increased in miners with heat cramps compared with miners without this symptom (p < 0.001), but there was no significant difference in sodium concentration (p = 0.384). Mean psychrometric wet bulb temperature was 29.0 degrees C (SD 2.2, range 21.0-34.0). Mean dry bulb temperature was 37.4 degrees C (SD 2.4, range 31.0-43.0). Mean air velocity was 0.54 m/s (SD 0.57, range 0.00-4.00). Mean air cooling power was 148 W/m2 (SD 49, range 33-290) Mean psychrometric wet bulb globe temperature was 31.5 degrees C (SD 2.0, range 25.2-35.3). Few cases (< 5%) occurred at psychrometric wet bulb temperature < 25.0 degrees C, dry bulb temperature < 33.8 degrees C, air velocity > 1.56 m/s, air cooling power > 248 W/m2, or psychrometric wet bulb globe temperature < 28.5 degrees C. CONCLUSION: Heat exhaustion in underground miners is associated with dehydration, neutrophil leukocytosis, eosinopenia, metabolic acidosis, increased glucose and ferritin, and a mild rise in creatine kinase, aspartate transaminase, and lactate dehydrogenase. Heat cramps are associated with dehydration but not hyponatraemia. The incidence of heat exhaustion increases during summer and at depth. An increased fluid intake is required. Heat exhaustion would be unlikely to occur if ventilation and refrigeration achieved air cooling power > 250 W/m2 at all underground work sites. (+info)
Glucocorticoids reduce interleukin-1 concentration and result in neuroprotective effects in rat heatstroke.
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In urethane-anaesthetized rats, we assessed the protective effects of glucocorticoids against heatstroke-induced arterial hypotension and ischaemic neuronal damage. Heatstroke was induced by exposing the animals to an ambient temperature of 42 C. The time at which both the mean arterial pressure (MAP) and local cerebral blood flow (CBF) in the striatum decreased from their peak levels was taken as the onset of heatstroke. Control rats were exposed to a temperature of 24 C. The values of MAP and CBF after heatstroke onset were all significantly lower than those in control rats. However, the neuronal damage score in the striatum and serum levels of interleukin-1beta (IL-1beta) were greater. Systemic pretreatment or treatment with an exogenous glucocorticoid, dexamethasone (4 mg or 6 mg kg-1, i.v.), reduced the heatstroke-induced arterial hypotension, serum IL-1beta levels, cerebral ischaemia and neuronal damage, and resulted in prolongation of the time to death (TTD; the interval between the onset of heat stress and cardiac arrest). Following bilateral adrenalectomy, MAP, CBF and TTD values were found to be significantly lower in the adrenalectomized (ADX) rats than in the sham-ADX rats after heat exposure. These changes were attenuated by dexamethasone. The data support the argument that glucocorticoids reduce the plasma IL-1beta concentration and may provide the neuroprotective effects observed in rat heatstroke. (+info)
Heat related mortality in warm and cold regions of Europe: observational study.
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OBJECTIVES: To assess heat related mortalities in relation to climate within Europe. DESIGN: Observational population study. SETTING: North Finland, south Finland, Baden-Wurttemberg, Netherlands, London, north Italy, and Athens. SUBJECTS: People aged 65-74. MAIN OUTCOME MEASURES: Mortalities at temperatures above, below, and within each region's temperature band of minimum mortality. RESULTS: Mortality was lowest at 14.3-17.3 degrees C in north Finland but at 22.7-25.7 degrees C in Athens. Overall the 3 degrees C minimum mortality temperature bands were significantly higher in regions with higher than lower mean summer temperatures (P=0.027). This was not due to regional differences in wind speeds, humidity, or rain. As a result, regions with hot summers did not have significantly higher annual heat related mortality per million population than cold regions at temperatures above these bands. Mean annual heat related mortalities were 304 (95% confidence interval 126 to 482) in North Finland, 445 (59 to 831) in Athens, and 40 (13 to 68) in London. Cold related mortalities were 2457 (1130 to 3786), 2533 (965 to 4101), and 3129 (2319 to 3939) respectively. CONCLUSIONS: Populations in Europe have adjusted successfully to mean summer temperatures ranging from 13.5 degrees C to 24.1 degrees C, and can be expected to adjust to global warming predicted for the next half century with little sustained increase in heat related mortality. Active measures to accelerate adjustment to hot weather could minimise temporary rises in heat related mortality, and measures to maintain protection against cold in winter could permit substantial reductions in overall mortality as temperatures rise. (+info)
Nitric oxide does not contribute to the hypotension of heatstroke.
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The purpose of this study was to determine whether nitric oxide (NO) contributes to the hypotensive state induced by prolonged environmental heat (EH) stress. Ketamine-anesthetized rats were instrumented for the measurement of arterial blood pressure, electrocardiogram, and temperature at four sites. Rats were exposed to EH (ambient temperature, 40 +/- 1 degrees C) until mean arterial blood pressure (MAP) decreased to 75 mmHg, which was arbitrarily defined as the induction of heatstroke. In addition to cardiovascular and temperature measurements, the time required to reach this MAP end point and the subsequent survival time were measured. In three separate experimental series, the competitive NO synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was administered (0, 10, or 100 mg/kg) either before, during (30 min after initiation of EH), or immediately after EH. L-NAME administered at any of these times transiently increased MAP. L-NAME infusion either before or during EH did not alter the EH time required to decrease MAP to 75 mmHg, but L-NAME pretreatment did decrease the colonic temperature at which this MAP end point was reached. L-NAME infusion before or after EH did not affect subsequent survival time, but L-NAME administered during EH significantly decreased survival time. The administration of L-NAME at any time point, therefore, did not prove beneficial in either preventing or reversing heatstroke. Taken together, these data suggest that NO does not mediate the hypotension associated with heatstroke. (+info)
Environmental factors and heatstroke.
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The objective of this study was to determine the extent of the influence of temperature and humidity on the number of heatstroke presentations. Three hundred and forty-five labourers presented to the Accident and Emergency Hospital in Abu Dhabi with heatstroke during a 3 month summer period. There was no significant predictive association between the maximum daily temperature and/or humidity and the presentation of heatstroke. There was no significant association with the maximum temperature on the previous day, day of the week or temperature trend. The largest statistical correlation was between the maximum temperature and humidity and the log of the number of cases. It is possible that there are other significant explanatory variables that we have not included in the model. (+info)