Within the global warming context, heat stroke heavily threatens human health as the most severe type of heat-related illnesses. Despite the urgent onset, severe condition and poor prognosis, heat stroke is entirely preventable and treatable. Most of the recipient countries of Chinese foreign medical aid work are concentrated in the tropical and subtropical regions. It is necessary to popularize the knowledge of heat stroke and improve the ability of diagnose and treatment among foreign medical aid members, which is critical to enhance the quality of medical service and provide better medical care for recipient countries and workers in Chinese-funded institutions. This article reviews the latest research progress in the epidemiology, pathophysiology, diagnosis, and treatment of heat stroke to provide scientific reference for actively implementing interventions and reducing morbidity and mortality.
China ; Global Warming ; Heat Stress Disorders/therapy* ; Heat Stroke/prevention & control* ; Humans ; Morbidity

Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Heat Stress Disorders ; drug therapy ; metabolism ; Hypothalamus ; metabolism ; Male ; Neurotensin ; metabolism ; Phytotherapy ; Rats ; Rats, Wistar ; Tablets

OBJECTIVETo study whether previously intravenous injection of anisodamine can prevent endotoxemia of heat stroke of rats.

METHODSExperimental animals were randomly divided into two groups, their average artery pressure, heart rate, survival time, survival rate and rectal temperature were measured at an environmental temperature of 38 degrees C-40 degrees C and 50%-60% retative humidity. Blood samples for endotoxins analyses were taken both before and after heat-stress.

RESULTSDuring heat stress, the animals of rectal temperature of the experimental and control groups continuously increased and two hours later, separately to (42.7 +/- 0.6) degree C and (43.1 +/- 0.5) degree C, without statistic difference(P > 0.05), and to (44.6 +/- 0.4) degree C and (44.2 +/- 0.3) degree C prior to death, with statistic difference(P < 0.05). Before the experiment, the contents of endotoxins of portal vein blood were (45.7 +/- 5.2) pg/ml and (42.6 +/- 5.4) pg/ml, and that of systemic blood was (14.8 +/- 4.5) pg/ml and (13.9 +/- 7.2) pg/ml, without statistic difference(P > 0.05). Two hours later, the contents of portal vein blood separately increased to (122.2 +/- 16.7) pg/ml and (49.7 +/- 10.2) pg/ml, obviously higher than that before heat-stress(P < 0.01). And there were clear statistic difference between the two groups(P < 0.01). The changing tendency of the heart rhythm is almost the same in two groups, that is, first rose and then fell. But it is without statistic difference before and two hours later(P > 0.05): before heat-stress, the average artery pressures were (13.3 +/- 0.6) kPa and (13.6 +/- 0.5) kPa, without statistic difference(P > 0.05), and two hours later, were (9.6 +/- 0.5) kPa and (8.6 +/- 0.6) kPa, with obvious statistic difference(P < 0.01). The survival time of the animals were (166.5 +/- 16.9) min and (144.5 +/- 18.2) min with obvious statistic difference(P < 0.01), the survival rate of heat stressed rats in the experimental group were obviously higher than control group(P < 0.01 or P < 0.05).

CONCLUSIONSAnisodamine can prevent endotoxemia in rats suffering heat stroke.

Animals ; Blood Pressure ; Body Temperature ; Endotoxemia ; prevention & control ; Endotoxins ; blood ; Heat Stress Disorders ; drug therapy ; mortality ; physiopathology ; Hot Temperature ; Rats ; Solanaceous Alkaloids ; therapeutic use ; Survival Rate

Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperature rise caused by heat stress, but the mechanism responsible for the BBR effect on HSP70 and TNFα signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNFα and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNFα were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNFα were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNFα homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNFα. Furthermore, TNFα could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNFα by suppressing their gene transcription, thereby decreasing body temperature under heat conditions. In conclusion, BBR has a potential to be developed as a therapeutic strategy for suppressing the thermal effects in hot environments.
Animals ; Berberine ; pharmacology ; HSP70 Heat-Shock Proteins ; genetics ; metabolism ; Heat Stress Disorders ; drug therapy ; genetics ; metabolism ; Hot Temperature ; Humans ; Male ; Mice ; Mice, Inbred ICR ; TATA Box ; drug effects ; Tumor Necrosis Factor-alpha ; genetics ; metabolism