Heat Tolerance: A Role for Fever?

Hales, J. R. S.; Sakurada, Sotaro

doi:10.1111/j.1749-6632.1998.tb08326.x

Cited by 20 publications

(22 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, only 32.6% of civilian (48) and 35% of military (49) heat stroke patients are hypotensive. The concentrations of inflammatory cytokines are increased and endotoxemia is present in heat stroke patients (4,7,24,43). In animals, some experiments used the achievement of a high T c as the criterion for inducing heat stroke.…”

Section: Discussionmentioning

confidence: 99%

“…The current model suggests that heat stroke is triggered by circulatory and thermoregulatory collapse during hyperthermia and driven by endotoxemia (6,24,43). Endotoxemia refers to an elevated level of gram-negative bacterial endotoxin, known as LPS, in the circulation (43).…”

mentioning

confidence: 99%

“…The secretion of these proinflammatory cytokines induces the production of IL-6, an inflammatory-responsive cytokine (4,7). The role of IL-6 during heat stroke is significant because the concentration of IL-6 is positively associated with the severity of the heat stroke (4,6,24,43). In animal studies, the concentrations of IL-1␤ in the brain and serum are elevated during heat stroke in rats (13,38,39) and rabbits (37) that develop arterial and cerebral hypotension and cardiovascular instability.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

Lim¹,

Wilson²,

Brown³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (TϩHE), dexamethasone (DϩHE), and turpentine and dexamethasone combined (TDϩHE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T c) was 42°C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T c 40°C (T40), and 15 min after achieving T c 42°C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TDϩHE rats (37.5%), followed by the HE (62.5%), TϩHE (75%), and DϩHE (100%) rats (P Ͻ 0.05). The duration of survival at T42°C was shortest in the TDϩHE rats (9.9 Ϯ 6.2 min) (P Ͻ 0.01), followed by the TϩHE (11.3 Ϯ 6.1 min) and the HE (12.2 Ϯ 4 min) (P Ͻ 0.05) rats. The increase in plasma IL-6 concentrations was highest in the TϩHE (352%) and HE (178%) rats (P Ͻ 0.05). DϩHE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

Lim¹,

Wilson²,

Brown³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…It has been suggested that hyperthermia during heat exposure results from an inability to dissipate heat as well as an increase in the temperature set point that initiates fever in response to endotoxin leakage from damaged gut membranes (143,144). Fever in combination with heat exposure will accelerate the increase in body temperature resulting in more rapid collapse to heat stroke.…”

Section: Gut Epithelial Permeability and Bacterial Translocationmentioning

confidence: 98%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

360

356

View full text Add to dashboard Cite

Heat stroke is a life-threatening condition clinically diagnosed as a severe elevation in body temperature with central nervous system dysfunction that often includes combativeness, delirium, seizures, and coma. Classic heat stroke primarily occurs in immunocompromised individuals during annual heat waves. Exertional heat stroke is observed in young fit individuals performing strenuous physical activity in hot or temperature environments. Long-term consequences of heat stroke are thought to be due to a systemic inflammatory response syndrome. This article provides a comprehensive review of recent advances in the identification of risk factors that predispose to heat stroke, the role of endotoxin and cytokines in mediation of multi-organ damage, the incidence of hypothermia and fever during heat stroke recovery, clinical biomarkers of organ damage severity, and protective cooling strategies. Risk factors include environmental factors, medications, drug use, compromised health status, and genetic conditions. The role of endotoxin and cytokines is discussed in the framework of research conducted over 30 years ago that requires reassessment to more clearly identify the role of these factors in the systemic inflammatory response syndrome. We challenge the notion that hypothalamic damage is responsible for thermoregulatory disturbances during heat stroke recovery and highlight recent advances in our understanding of the regulated nature of these responses. The need for more sensitive clinical biomarkers of organ damage is examined. Conventional and emerging cooling methods are discussed with reference to protection against peripheral organ damage and selective brain cooling.

show abstract

“…These proinXammatory cytokines induce production of IL-6, which is positively associated with the severity of the heatstroke (Hales and Sakurada 1998;Moseley and GisolW 1993). IL-1ra is a potent and highly selective, competitive IL-1 antagonist, which is able to block all actions of IL-1 and is also induced by tissue damage (Hannum et al 1990;Loddick et al 1997;Pinteaux et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-1 receptor antagonist restores homeostatic function and limits multiorgan damage in heatstroke

et al. 2008

View full text Add to dashboard Cite

We attempt to investigate whether interleukin-1 receptor antagonist (IL-1ra) therapy improves survival during heatstroke by attenuating multiorgan dysfunction. Anesthetized rabbits, immediately after the onset of heatstroke, are divided into three major groups and given: nothing, normal saline (1 ml/kg, i.v.), or IL-1ra (200-400 microg per 1 ml/kg, i.v.). They are exposed to ambient temperature of 40 degrees C to induce heatstroke. Another group of rabbits is exposed to room temperature (24 degrees C) and used as normothermic controls. Hyperthermia, hypotension, cerebral ischemia and edema, hepatic and renal failure, increased levels of both nitric oxide metabolites (NO ( x ) (-) ) and dihydroxybenzoic acid (DHBA) in plasma, hyperkalemia, respiratory alkalosis, and metabolic acidosis and hypoxia are all observed in vehicle-treated heatstroke animals. When the vehicle-treated animals undergo heat stress, their survival time values are found to be 12-18 min. Resuscitation with IL-1ra dose-dependently improves survival time (duration, 132-303 min). As compared with vehicle-treated heatstroke rabbits, IL-1ra therapy significantly causes attenuation of heatstroke-induced hyperthermia, hypotension, cerebral ischemia and edema, intracranial hypertension, hepatic and renal dysfunction, NO ( x ) (-) and DHBA overproduction, hyperkalemia, hypoxia, respiratory alkalosis, and metabolic acidosis. The results indicate that IL-1ra therapy may restore tissue blood flow and homeostatic function, and limit multiorgan dysfunction and death in heatstroke.

show abstract

Heat Tolerance: A Role for Fever?

Cited by 20 publications

References 51 publications

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

Heat Stroke

Interleukin-1 receptor antagonist restores homeostatic function and limits multiorgan damage in heatstroke

Contact Info

Product

Resources

About