Dantrolene sodium for treatment of heatstroke victims: Lack of efficacy in a canine model

Amsterdam, James T.; Syverud, Scott A.; Barker, William J.; Bills, Gordon R.; Goltra, David D.; Armao, Joseph C.; Hedges, Jerris R.

doi:10.1016/0735-6757(86)90186-5

Cited by 24 publications

(11 citation statements)

References 26 publications

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“…• C), but failed to show an effect on cooling rate, hemoconcentration, prothrombin time (one of several clinical measures of disseminated intravascular coagulation; DIC), mean arterial blood gas responses, serum chemistries, or organ damage through 12 h of recovery (15). Similarly, therapeutic intervention of an immature pig heat stroke model (body temperature = 43…”

Section: Malignant Hyperthermiamentioning

confidence: 94%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

346

356

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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.

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Section: Malignant Hyperthermiamentioning

confidence: 94%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

346

356

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“…8 Dantrolene is now the drug of choice to treat malignant hyperthermia 10 • 11 It has also been reported effective in the treatment of heat stroke, but an experimental study in canines did not show its efficacy in the treatment of nonexertional heat stroke. 12 One study showed that patients with malignant hyperthermia demonstrate minor abnormalities of heat dissipation. 13 A study of 630 members of a Nebraska family (including ancestors) with a high incidence of malignant hyperthermia revealed several members with the malignant hyperthermia trait who had heatrelated problems.…”

mentioning

confidence: 98%

Malignant Hyperthermia in a College Football Player

Hunter¹,

Rosenberg²,

Tuttle³

et al. 1987

The Physician and Sportsmedicine

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“…Heat acclimatization is specific to the type of environment and physical activity level, but exposure to one environment (e.g., desert) can improve exercise capabilities in other hot environments (e.g., jungle; [343,414]). To achieve heat acclimation, heat exposures need to be sufficiently stressful to elevate both core [16] and skin temperature [330] with profuse sweating [26,318]. The functional outcomes of heat acclimatization include thermoregulatory, cardiovascular, metabolic, and fluid-electrolyte adaptations (Table 3).…”

Section: Heat Acclimatizationmentioning

confidence: 99%

“…Improved monitoring standards, early detection, and dantrolene treatment has significantly increased survival compared to the untreated condition [247]. For example, dantrolene had no effect on cooling rate, hemoconcentration, coagulation biomarkers, or organ injury in an anesthetized canine model of exertional heat stroke [16]. It has been suggested that excessive Ca 2+ release from the RyR1 is an underlying etiology for exertional heat stroke based on the responses of a small subset (~5-10%) of MH patients and animal models that develop reactions to exercise, heat exposure, and emotional stress [95,411].…”

Section: Malignant Hyperthermiamentioning

confidence: 99%

Pathophysiology of Heat Stroke

Leon¹

2015

Colloquium Series on Integrated Systems Physiology: From Molecule to Function

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Dantrolene sodium for treatment of heatstroke victims: Lack of efficacy in a canine model

Cited by 24 publications

References 26 publications

Heat Stroke

Heat Stroke

Malignant Hyperthermia in a College Football Player

Pathophysiology of Heat Stroke

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