Hyperbaric oxygen preconditioning normalizes scrotal temperature, sperm quality, testicular structure, and erectile function in adult male rats subjected to exertional heat injury.

Testicular hyperthermia has been noted in men who work in high ambient temperatures. Scrotal temperatures above the normal range caused germ cell loss in the testes and resulted in male subfertility. In adult male rats, exercising at a higher environmental temperature (36 °C with relative humidity of 50%, 52 min) caused exertional heat stroke (EHS) characterized by scrotal hyperthermia, impaired sperm quality, dysmorphology in testes, prostates and bladders, and erectile dysfunction. Here, we aim to ascertain whether hyperbaric oxygen preconditioning (HBOP: 100% O2 at 2.0 atm absolute [ATA] for 2 h daily for 14 days consequently before the onset of EHS) is able to prevent the problem of EHS-induced sterility, testes, prostates, and bladders dysmorphology and erectile dysfunction. At the end of exertional heat stress compared to normobaric air (NBA or non-HBOP) rats, the HBOP rats exhibited lower body core temperature (40 °C vs. 43 °C), lower scrotal temperature (34 °C vs. 36 °C), lower neurological severity scores (2.8 vs. 5.8), higher erectile ability, (5984 mmHg-sec vs. 3788 mmHg-sec), higher plasma testosterone (6.8 ng/mL vs. 3.5 ng/mL), lower plasma follicle stimulating hormone (196.3 mIU/mL vs. 513.8 mIU/mL), lower plasma luteinizing hormone (131 IU/L vs. 189 IU/L), lower plasma adrenocorticotropic hormone (5136 pg/mL vs. 6129 pg/mL), lower plasma corticosterone (0.56 ng/mL vs. 1.18 ng/mL), lower sperm loss and lower values of histopathological scores for epididymis, testis, seminal vesicle, prostate, and bladder. Our data suggest that HBOP reduces body core and scrotal hyperthermia and improves sperm loss, testis/prostate/bladder dysmorphology, and erectile dysfunction after EHS in rats.

[Study on drug properties of Arisaematis Rhizoma and Arisaema Cum Bile based on substance and energy metabolism in normal and cold/heat syndrome model rats].

This paper clarified the scientific connotation of the changes in cold and heat properties of Arisaematis Rhizoma and Arisaema Cum Bile through investigating the changes of substance and energy metabolism after drug intervention in the rats with normal and cold/heat syndrome, so as to improve the method of evaluating the drug properties of Chinese medicine. After one week of adaptive feeding, healthy male SD rats were randomly divided into three parts: normal rats, heat syndrome rat models, and cold syndrome rat models. Through ice water bath and oral euthyrox(120 µg·kg~(-1)), the models of cold syndrome and heat syndrome were induced, respectively. The models were made at 9:00 am. and administrated by gavage at 3:00 pm. every day. All administration groups were administrated with Arisaematis Rhizoma and Arisaema Cum Bile decoction, respectively, and the blank group was given the same dose of normal saline. After continuous administration for 15 d, the rats were anesthetized by chloral hydrate, blood was taken from abdominal aorta, and the hearts and livers were removed and stored at-80 ℃. The changes in the body weight and anal temperature of rats during administration were detected, and the liver coefficient of rats was detected after removing the liver. Enzyme-linked immunosorbent assay(ELISA) was adopted to detect the expression level of the indexes related to substance and energy metabolism in liver and heart of rat, and Western blot was used to detect the expression of key proteins in AMPK/mTOR signaling pathway for further verification. The results showed that Arisaematis Rhizoma enhanced the expression level of enzymes related to substance and energy metabolism in the normal and cold and heat syndrome rat models, and increased anal temperature, which exhibited warm(hot) drug property. Arisaema Cum Bile inhibited the level of substance and energy metabolism in rats, and reduced anal temperature, which showed cold(cool) drug property. Chinese Pharmacopoeia has recorded "Arisaematis Rhizoma has warm property and Arisaema Cum Bile has cool property", which is consistent with the phenomenon in this study. Therefore, it is feasible to evaluate the drug properties of Chinese medicine based on the substance and energy metabolism of normal and cold/heat syndrome model rats, which completes the method of evaluating drug properties of Chinese medicine.

Hypobaric hypoxia preconditioning protects against hypothalamic neuron apoptosis in heat-exposed rats by reversing hypothalamic overexpression of matrix metalloproteinase-9 and ischemia.

Background: Hypoxia-inducible factor-1α (HIF-1α), heat shock protein-72 (HSP-72), hemeoxygenase-1 (HO-1), and matrix metalloproteinase-9 (MMP-9) have been identified as potential therapeutic targets in the brain for cerebral ischemia. To elucidate their underlying mechanisms, we first aimed to ascertain whether these proteins participate in the pathogenesis of heat-induced ischemic damage to the hypothalamus of rats. Second, we investigated whether hypobaric hypoxia preconditioning (HHP) attenuates heat-induced hypothalamic ischemic/hypoxic injury by modulating these proteins in situ. Methods: Anesthetized rats treated with or without HHP were subjected to heat stress. Hypothalamic ischemic/hypoxic damage was evaluated by measuring hypothalamic levels of cerebral blood flow (CBF), partial oxygen pressure (PO2), and hypothalamic temperature via an implanted probe. Hypothalamic apoptotic neurons were counted by measuring the number of NeuN/caspase-3/DAPI triple-stained cells. Hypothalamic protein expression of HIF-1α, HSP-72, HO-1, and MMP-9 was determined biochemically. Results: Before the start of the thermal experiments, rats were subjected to 5 hours of HHP (0.66 ATA or 18.3% O2) daily for 5 consecutive days per week for 2 weeks, which led to significant loss of body weight, reduced brown adipose tissue (BAT) wet weight and decreased body temperature. The animals were then subjected to thermal studies. Twenty minutes after heat stress, heat-exposed rats not treated with HHP displayed significantly higher core and hypothalamic temperatures, hypothalamic MMP-9 levels, and numbers of hypothalamic apoptotic neurons but significantly lower mean blood pressure, hypothalamic blood flow, and PO2 values than control rats not exposed to heat. In heat-exposed rats, HHP significantly increased the hypothalamic levels of HIF-1α, HSP-72, and HO-1 but significantly alleviated body and hypothalamic hyperthermia, hypotension, hypothalamic ischemia, hypoxia, neuronal apoptosis and degeneration. Conclusions: HHP may protect against hypothalamic ischemic/hypoxic injury and overexpression of MMP-9 by upregulating the hypothalamic expression of HIF-1α, HSP-72, and HO-1 in rats subjected to heatstroke.

The Gastrointestinal Exertional Heat Stroke Paradigm: Pathophysiology, Assessment, Severity, Aetiology and Nutritional Countermeasures.

Exertional heat stroke (EHS) is a life-threatening medical condition involving thermoregulatory failure and is the most severe condition along a continuum of heat-related illnesses. Current EHS policy guidance principally advocates a thermoregulatory management approach, despite growing recognition that gastrointestinal (GI) microbial translocation contributes to disease pathophysiology. Contemporary research has focused to understand the relevance of GI barrier integrity and strategies to maintain it during periods of exertional-heat stress. GI barrier integrity can be assessed non-invasively using a variety of in vivo techniques, including active inert mixed-weight molecular probe recovery tests and passive biomarkers indicative of GI structural integrity loss or microbial translocation. Strenuous exercise is strongly characterised to disrupt GI barrier integrity, and aspects of this response correlate with the corresponding magnitude of thermal strain. The aetiology of GI barrier integrity loss following exertional-heat stress is poorly understood, though may directly relate to localised hyperthermia, splanchnic hypoperfusion-mediated ischemic injury, and neuroendocrine-immune alterations. Nutritional countermeasures to maintain GI barrier integrity following exertional-heat stress provide a promising approach to mitigate EHS. The focus of this review is to evaluate: (1) the GI paradigm of exertional heat stroke; (2) techniques to assess GI barrier integrity; (3) typical GI barrier integrity responses to exertional-heat stress; (4) the aetiology of GI barrier integrity loss following exertional-heat stress; and (5) nutritional countermeasures to maintain GI barrier integrity in response to exertional-heat stress.

Exertional Heat Stroke: Pathophysiology, Epidemiology, Diagnosis, Treatment, and Prevention.

Temperature increases due to climate changes and operations expected to be conducted in hot environments make heat-related injuries a major medical concern for the military. The most serious of heat-related injuries is exertional heat stroke (EHS). EHS generally occurs when health individual perform physical activity in hot environments and the balance between body heat production and heat dissipation is upset resulting in excessive body heat storage. Blood flow to the skin is increased to assist in dissipating heat while gut blood flow is considerably reduced, and this increases the permeability of the gastrointestinal mucosa. Toxic materials from gut bacteria leak through the gastrointestinal mucosa into the central circulation triggering an inflammatory response, disseminated intravascular coagulation (DIC), multiorgan failure, and vascular collapse. In addition, high heat directly damages cellular proteins resulting in cellular death. In the United States military, the overall incidence of clinically diagnosed heat stroke from 1998 to 2017 was (mean ± standard deviation) 2.7 ± 0.5 cases/10,000 Soldier-years and outpatient rates rose over this period. The cornerstone of EHS diagnosis is recognition of central nervous dysfunction (ataxia, loss of balance, convulsions, irrational behavior, unusual behavior, inappropriate comments, collapse, and loss of consciousness) and a body core temperature (obtained with a rectal thermometer) usually >40.5°C (105°F). The gold standard treatment is whole body cold water immersion. In the field where water immersion is not available it may be necessary to use ice packs or very cold, wet towels placed over as much of the body as possible before transportation of the victim to higher levels of medical care. The key to prevention of EHS and other heat-related injuries is proper heat acclimation, understanding work/rest cycles, proper hydration during activity, and assuring that physical activity is matched to the Soldiers' fitness levels. Also, certain dietary supplements (DSs) may have effects on energy expenditure, gastrointestinal function, and thermoregulation that should be considered and understood. In many cases over-motivation is a major risk factor. Commanders and trainers should be alert to any change in the Soldier's behavior. Proper attention to these factors should considerably reduce the incidence of EHS.

Hypothalamic impairment underlying heat intolerance in pregnant mice.

Pregnant women are vulnerable to heat stroke reactions caused by high environmental temperatures. Heat intolerance is associated with hypothalamic impairment. Here, we aim to ascertain whether pregnancy causes heat intolerance by inducing hypothalamic impairment in mice. In the heated groups, mice were exposed to whole body heating (WBH; 41.2 °C for 1 h) in an environment-controlled chamber. Then, they were returned to normal room temperature (26 °C) immediately after WBH. In the hyperbaric oxygen therapy (HBO2T) groups, mice were exposed to 100% O2 at 2.0 atm absolute (ATA) for 4 h immediately post-WBH. Mice that survived after 4 h of WBH were considered survivors. Here, we show that when pregnant mice underwent non-HBO2T (21% O2 at 1.0 ATA for 4 h) after WBH, the survival rate was 4/20, and the core temperature at 4 h post-WBH was 31.2 ±â€¯0.2 °C. Both the survival rate and core temperature of HBO2T pregnant mice (10/10 and 35.2 ±â€¯0.3 °C, respectively) were significantly greater than those in non-HBO2T pregnant mice. Compared to non-HBO2T heated mice, the HBO2T heated mice exhibited lower neurological severity scores, reduced hypothalamic neuronal damage, fewer apoptotic cells, reduced multiorgan damage scores, and lower hypothalamic levels of proinflammatory cytokines and nitrogen and oxygen radical species. Compared to non-HBO2T heated mice, the HBO2T-treated heated mice had significantly higher hypothalamic-pituitary-adrenal axis activity (evidenced by higher serum levels of both adrenocorticotrophic hormone and corticosterone). In conclusion, pregnancy induces heat intolerance by inducing hypothalamic impairment in mice. Additionally, HBO2T protects against heat intolerance in pregnant mice by preserving hypothalamic integrity.

Are Recommended Heat Stroke Treatments Adequate for Australian Workers?

Workers that combine physical exertion with exposure to hot conditions are susceptible to heat-related illnesses, including heat stroke. Despite recognition of cold water immersion as the heat stroke treatment of choice in the peer-reviewed literature, it was not included within recommended treatments of leading Australian healthcare training organizations and was omitted from Safe Work Australia's recently updated 'Managing the risks of working in heat' guidance material. On this basis, the guidance material appears an opportunity lost to assist Australian industry transition their heat stroke management to reflect the evidence. It is recommended that Australian providers of healthcare training, and those reliant on such information, review the efficacy of their heat stroke treatments.

Cooling Rates of Hyperthermic Humans Wearing American Football Uniforms When Cold-Water Immersion Is Delayed.

CONTEXT: Treatment delays can be contributing factors in the deaths of American football athletes from exertional heat stroke. Ideally, clinicians begin cold-water immersion (CWI) to reduce rectal temperature (Trec) to <38.9°C within 30 minutes of collapse. If delays occur, experts recommend Trec cooling rates that exceed 0.15°C/min. Whether treatment delays affect CWI cooling rates or perceptual variables when football uniforms are worn is unknown. OBJECTIVE: To answer 3 questions: (1) Does wearing a football uniform and delaying CWI by 5 minutes or 30 minutes affect Trec cooling rates? (2) Do Trec cooling rates exceed 0.15°C/min when treatment delays have occurred and individuals wear football uniforms during CWI? (3) How do treatment delays affect thermal sensation and Environmental Symptoms Questionnaire responses? DESIGN: Crossover study. SETTING: Laboratory. PATIENTS OR OTHER PARTICIPANTS: Ten physically active men (age = 22 ± 2 y, height = 183.0 ± 6.9 cm, mass = 78.9 ± 6.0 kg). INTERVENTION(S): On 2 days, participants wore American football uniforms and exercised in the heat until Trec was 39.75°C. Then they sat in the heat, with equipment on, for either 5 or 30 minutes before undergoing CWI (10.6°C ± 0.1°C) until Trec reached 37.75°C. MAIN OUTCOME MEASURE(S): Rectal temperature and CWI duration were used to calculate cooling rates. Thermal sensation was measured pre-exercise, postexercise, postdelay, and post-CWI. Responses to the Environmental Symptoms Questionnaire were obtained pre-exercise, postdelay, and post-CWI. RESULTS: The Trec cooling rates exceeded recommendations and were unaffected by treatment delays (5-minute delay = 0.20°C/min ± 0.07°C/min, 30-minute delay = 0.19°C/min ± 0.05°C/min; P = .4). Thermal sensation differed between conditions only postdelay (5-minute delay = 6.5 ± 0.6, 30-minute delay = 5.5 ± 0.7; P < .05). Environmental Symptoms Questionnaire responses differed between conditions only postdelay (5-minute delay = 27 ± 15, 30-minute delay = 16 ± 12; P < .05). CONCLUSIONS: Treatment delays and football equipment did not impair CWI's effectiveness. Because participants felt cooler and better after the 30-minute delay despite still having elevated Trec, clinicians should use objective measurements (eg, Trec) to guide their decision making for patients with possible exertional heat stroke.

Liver Injury Associated with Sporting Activities.

Exertional heat stroke most commonly develops following prolonged levels of aerobic activity in a warm or humid environment. Hypoperfusion of the vital organs along with activation of the inflammasome can lead to progressive and potentially fatal multiorgan failure including acute liver failure. In the United States, herbal and dietary supplements that are marketed to improve performance, strength, and weight loss are increasingly being used by both amateur and professional athletes. Consumption of bodybuilding supplements that contain androgenic anabolic steroids can lead to adverse hepatic effects ranging from asymptomatic serum aminotransferase elevations to severe cholestatic hepatitis with prolonged jaundice. Various non-bodybuilding nutritional supplements that contain a mixture of botanicals, caffeine, and chemicals have also been associated with idiosyncratic hepatotoxicity. In particular, green tea extract derivatives that contain epigallocatechin gallate are hepatotoxic in animal models and have been associated with severe acute hepatocellular injury in humans.

Umbilical cord blood-derived stem cells improve heat tolerance and hypothalamic damage in heat stressed mice.

Heatstroke is characterized by excessive hyperthermia associated with systemic inflammatory responses, which leads to multiple organ failure, in which brain disorders predominate. This definition can be almost fulfilled by a mouse model of heatstroke used in the present study. Unanesthetized mice were exposed to whole body heating (41.2°C for 1 hour) and then returned to room temperature (26°C) for recovery. Immediately after termination of whole body heating, heated mice displayed excessive hyperthermia (body core temperature ~42.5°C). Four hours after termination of heat stress, heated mice displayed (i) systemic inflammation; (ii) ischemic, hypoxic, and oxidative damage to the hypothalamus; (iii) hypothalamo-pituitary-adrenocortical axis impairment (reflected by plasma levels of both adrenocorticotrophic-hormone and corticosterone); (iv) decreased fractional survival; and (v) thermoregulatory deficits (e.g., they became hypothermia when they were exposed to room temperature). These heatstroke reactions can be significantly attenuated by human umbilical cord blood-derived CD34(+) cells therapy. Our data suggest that human umbilical cord blood-derived stem cells therapy may improve outcomes of heatstroke in mice by reducing systemic inflammation as well as hypothalamo-pituitary-adrenocortical axis impairment.

Attenuating brain inflammation, ischemia, and oxidative damage by hyperbaric oxygen in diabetic rats after heat stroke.

BACKGROUND/PURPOSE: Alternating hypothalamic-pituitary-adrenal axis mechanisms would lead to multiple organs dysfunction or failure. Herein, we attempt to assess whether hypothalamic inflammation and ischemic and oxidative damage that occurred during heatstroke (HS) can be affected by hyperbaric oxygen (HBO2) therapy in streptozotocin-induced diabetic rats. METHODS: In this study, anesthetized diabetic rats, immediately after the onset of HS, were divided into two major groups and given the normobaric air (21% O2 at 1.0 atmospheres absolute) or HBO2 (100% O2 at 2.0 atmospheres absolute). HS was induced by exposing the animals to heat stress (43°C). Another group of anesthetized diabetic rats was kept at normothermic state and used as controls. RESULTS: The survival time values for the HBO2-treated HS-diabetic rats increased form the control values of 78-82 minutes to new values of 184-208 minutes. HBO2 therapy caused a reduction of HS-induced cellular ischemia (e.g., increased cellular levels of glutamate and lactate/pyruvate ratio), hypoxia (e.g., decreased cellular levels of PO2), inflammation (e.g., increased cellular levels of interleukin-1ß, tumor necrosis factor-alpha, interleukin-6, and myeloperoxidase), and oxidative damage (e.g., increased values of nitric oxide, 2,3-dihydroxybenzoic acid, glycerol, and neuronal damage score) in the hypothalamus of the diabetic rats. CONCLUSION: Our results suggest that, in diabetic animals, HBO2 therapy may improve outcomes of HS in part by reducing heat-induced activated inflammation and ischemic and oxidative damage in the hypothalamus and other brain regions.

Electrical vagus nerve stimulation attenuates systemic inflammation and improves survival in a rat heatstroke model.

This study was performed to gain insights into novel therapeutic approaches for the treatment of heatstroke. The central nervous system regulates peripheral immune responses via the vagus nerve, the primary neural component of the cholinergic anti-inflammatory pathway. Electrical vagus nerve stimulation (VNS) reportedly suppresses pro-inflammatory cytokine release in several models of inflammatory disease. Here, we evaluated whether electrical VNS attenuates severe heatstroke, which induces a systemic inflammatory response. Anesthetized rats were subjected to heat stress (41.5°C for 30 minutes) with/without electrical VNS. In the VNS-treated group, the cervical vagus nerve was stimulated with constant voltage (10 V, 2 ms, 5 Hz) for 20 minutes immediately after completion of heat stress. Sham-operated animals underwent the same procedure without stimulation under a normothermic condition. Seven-day mortality improved significantly in the VNS-treated group versus control group. Electrical VNS significantly suppressed induction of pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6 in the serum 6 hours after heat stress. Simultaneously, the increase of soluble thrombomodulin and E-selectin following heat stress was also suppressed by VNS treatment, suggesting its protective effect on endothelium. Immunohistochemical analysis using tissue preparations obtained 6 hours after heat stress revealed that VNS treatment attenuated infiltration of inflammatory (CD11b-positive) cells in lung and spleen. Interestingly, most cells with increased CD11b positivity in response to heat stress did not express α7 nicotinic acetylcholine receptor in the spleen. These data indicate that electrical VNS modulated cholinergic anti-inflammatory pathway abnormalities induced by heat stress, and this protective effect was associated with improved mortality. These findings may provide a novel therapeutic strategy to combat severe heatstroke in the critical care setting.

Reduction of ischemic and oxidative damage to the hypothalamus by hyperbaric oxygen in heatstroke mice.

The aims of the present paper were to ascertain whether the heat-induced ischemia and oxidative damage to the hypothalamus and lethality in mice could be ameliorated by hyperbaric oxygen therapy. When normobaric air-treated mice underwent heat treatment, the fractional survival and core temperature at 4 hours after heat stress were found to be 0 of 12 and 34 degrees C +/- 0.3 degrees C, respectively. In hyperbaric oxygen-treated mice, when exposed to the same treatment, both fractional survival and core temperature values were significantly increased to new values of 12/12 and 37.3 degrees C +/- 0.3 degrees C, respectively. Compared to normobaric air-treated heatstroke mice, hyperbaric oxygen-treated mice displayed lower hypothalamic values of cellular ischemia and damage markers, prooxidant enzymes, proinflammatory cytokines, inducible nitric oxide synthase-dependent nitric oxide, and neuronal damage score. The data indicate that hyperbaric oxygen may improve outcomes of heatstroke by normalization of hypothalamic and thermoregulatory function in mice.

Protection in rats with heatstroke: hyperbaric oxygen vs activated protein C therapy.

The present study was attempted to evaluate the therapeutic effects of activated protein C and/or hyperbaric oxygen in an animal model of heatstroke. Sixty-eight minutes heat stress (43 degrees C) initiated, the anesthetized rats were randomized to several groups and administered: 1) no resuscitation (vehicle solution plus normabaric air, 2) intravenous activated protein C (1mg in 1ml of normal saline per kg of body weight), 3) hyperbaric oxygen (100% oxygen at 202kpa for 17min), and 4) intravenous activated protein C plus hyperbaric oxygen. Another group of rats exposed to room temperature (26 degrees C) was used as normothermic controls. Blood sampling was 0min, 70min, and 85min after heat stress initiated. When the vehicle-treated rats underwent heat exposure, their survival time values found were to be 19-25min. Resuscitation with activated protein C or hyperbaric oxygen significantly and equally improved survival during heatstroke (134-159min). As compared with those of activated protein C or hyperbaric oxygen alone, combined activated protein C and hyperbaric oxygen significantly had higher survival time values (277-347min). All vehicle-treated heatstroke animals displayed systemic response, hypercoagulable state, and hepatic and renal dysfunction. Combined activated protein C and hyperbaric oxygen therapy reduced these heatstroke reactions better than activated protein C or hyperbaric oxygen alone. The results indicate consequently, combined activated protein C and hyperbaric oxygen therapy heightens benefit in combating heatstroke reactions.

Human umbilical cord blood cells protect against hypothalamic apoptosis and systemic inflammation response during heatstroke in rats.

BACKGROUND: Intravenous administration of human umbilical cord blood cells (HUCBC) has been shown to improve heatstroke by reducing arterial hypotension as well as cerebral ischemia and damage in a rat model. To extend these findings, we assessed both hypothalamic neuronal apoptosis and systemic inflammatory responses in the presence of HUCBCs or vehicle medium immediately after initiation of heatstroke. METHODS: Anesthetized rats, immediately after the initiation of heat stress, were divided into two groups and given either serum-free lymphocyte medium (0.3mL per rat, intravenously) or HUCBCs (5 x 10(6) in 0.3 mL serum-free lymphocyte medium, intravenously). Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Heatstroke was induced by exposing the anesthetized rats to a high ambient temperature of 43 degrees C for 68 minutes. RESULTS: After the onset of heatstroke, animals treated with serum-free lymphocyte medium displayed hyperthermia, hypotension, bradycardia, hypothalamic neuronal apoptosis and degeneration, and up-regulation of systemic inflammatory response molecules including serum tumor necrosis factor-alpha, soluble intercellular adhesion molecule-1 and E-selectin. Heatstroke-induced hypotension, bradycardia, hypothalamic neuronal apoptosis and degeneration, and increased systemic inflammatory response molecules were significantly inhibited by HUCBC treatment. Although heatstroke-induced hyperthermia was not affected by HUCBC treatment, the serum levels of the anti-inflammatory cytokine interleukin-10 were significantly increased by HUCBC therapy during hyperthermia. CONCLUSIONS: These findings suggest that HUCBC transplantation may prevent the occurrence of heatstroke by reducing hypothalamic neuronal damage and the systemic inflammatory responses.

A hyperbaric oxygen therapy approach to heat stroke with multiple organ dysfunction.

Here in we report the case of a patient who displayed a classic heat stroke with multiple organ dysfunction and hypercoagulable state resistant to conventional whole body cooling and antipyretic therapy, and necessitating the use of hyperbaric oxygen therapy (HBOT) to rescue him from death. A 49-year-old male laborer, suffering from heat stroke syndromes (e.g., hyperpyrexia, seizure and coma, and hypotension), was admitted to an emergency unit of a medical center hospital. The patient displayed multiple organ dysfunction with rhabdomyolysis, hepatic, renal, respiratory, and cerebral dysfunction, and disseminated intravascular coagulation (DIC). Both hyperpyrexia and multiple organ dysfunction were resistant to conventional treatment measures. HBOT was adopted to rescue the patient from heat stroke-induced death. Before HBOT, analyses of serum revealed hypercoagulable state or DIC as well as signs of rhabdomyolysis, and renal and hepatic failure. In addition, pulmonary edema, coma, hypotension, and hyperpyrexia occurred. HBOT was used successfully to combat these syndromes and to rescue the patient from heat stroke death. This case suggests that HBOT is useful for treatment of heat stroke with multiple organ dysfunction.

Cold-water dousing with ice massage to treat exertional heat stroke: a case series.

INTRODUCTION: We sought to determine the rate of cooling via a novel water ice therapy (WIT) as an alternative to cold-water immersion for the acute treatment of exertional heat stroke (EHS). METHODS: Observations were made at the 2004-2008 Marine Corps Marathons (mean +/- SD: 16.3 +/- 4.9 degrees C dry bulb, 32 +/- 6% RH). Nine (seven men, two women) EHS patients (33 +/- 6 yr of age; 268 +/- 54 min average race time for six who finished) were observed during on-site treatment. Patients were treated while lying supine on a porous stretcher resting on a tub filled with cold water (approximately 10-12 degrees C). Medical personnel monitored T(re), doused the patient with water and massaged major muscle groups with ice bags until T(re) decreased to 38.9 degrees C. Patients were not immersed in water. Serial T(re) and time were used to calculate cooling rates. RESULTS: Final T(re) (39.12 +/- 0.63 degrees C) was significantly lower than initial T(re) (41.43 +/- 0.71 degrees C, P < 0.05). Cooling rates were 0.13 +/- 0.04 degrees C min(-1). The decrease in T(re) for the initial 6 min of WIT (0.38 +/- 0.13 degrees C) was significantly less than for the subsequent 6-min time period (1.31 +/- 0.34 degrees C, P < 0.001). Cooling rates for these time periods were significantly different (0.06 +/- 0.02 degrees C x min(-1) and 0.22 +/- 0.06 degrees C x min(-1), respectively, P < 0.05). Initial T(re) was not correlated with overall cooling rate (r = 0.434, P = 0.244), or total cooling time required (17 +/- 4 min; r = 0.207, P = 0.593). Survival rate was 100%. CONCLUSION: WIT provided cooling rates that were 70% as effective as those published for cold-water immersion with 8 degrees C water (0.19 degrees C x min(-1)) and resulted in 100% patient survival.