Chapter 12 The effects of drugs on thermoregulation during exposure to hot environments

doi:10.1016/S0079-6123(08)62037-3

Progress in Brain Research

Volume 115, 1998, Pages 193-204

https://doi.org/10.1016/S0079-6123(08)62037-3 Get rights and content

Publisher Summary

During exposure to high ambient temperatures, the thermoregulatory centers in the brain and spinal cord activate appropriate physiological and behavioral responses to maintain the core temperature at the normal level of 37°C in the face of the external heat load. In addition to the hot environment, other factors have been implicated in the pathogenesis of classical heat stroke. Notable among these is the concomitant use of prescription drugs or exposure to exogenous chemicals, many of which are commonly used in agriculture and industry. Although there is evidence for secondary centers in the spinal cord, the major control of body temperature is exercised by neurones located in the rostra1 hypothalamus in the preoptic/anterior hypothalamic nuclear complex. The sites and mechanisms of action of exogenous substances, which interfere with normal temperature regulation, have been extensively studied in animals but far less completely in human subjects. The focus is primarily on brain function during heat exposure.

References (50)

E.W. Anderson et al.
Cardiovascular effects of benzedrine
Lancet
(1936)
R.E. Chipkin
Effects of D1 and D2 antagonists on basal and apomorphine decreased body temperature in mice and rats
Pharmacol. Biochem. Behav.
(1988)
W.G. Clark et al.
Drug related heatstroke
Pharmacol. Ther.
(1984)
W.G. Clark et al.
Changes in body temperature after administration of adrenergic and serotonergic agents and related drugs including antidepressants: II
Neurosci. Behav. Rev.
(1986)
B. Cox et al.
Dopaminergic involvement in withdrawal hypothermia and thermoregulatory behavior in morphine dependent rats
Pharmacol. Biochem. Behav.
(1976)
B. Cox et al.
Behavioral thermoregulation in the study of drugs affecting body temperature
Pharmacol. Biochem. Behav.
(1975)
M.A. Denborough
The pathophysiology of malignant hyperpyrexia
Pharmacol. Ther.
(1980)
W.E. Kirkpatrick et al.
Temperature changes induced by chlorpromazine and N-methyl chlorpromazine in the rat
Neuropharmacology
(1971)
P. Lomax et al.
Cocaine and body temperature in the rat: effect of exercise
Pharmacol. Biochem. Behav.
(1990)
T. Namba et al.
Poisoning due to organophosphate insecticides
Am. J. Med.
(1971)

D.L. Polk et al.

Effects of sodium salicylate, aminopyrine and chlorpromazine on behavioral temperature regulation

Pharmacol. Biochem. Behav.

(1975)

C. Sánchez

The effects of dopamine D-1 and D-2 receptors on body temperature in male mice

Eur. J. Pharmacol.

(1989)

M. Vasse et al.

The rise in body temperature induced by stimulation of dopamine D1 receptors is increased in acutely reserpinized mice

Eur. J. Pharmacol.

(1990)

J.M. Witkin et al.

Lethal effects of cocaine are reduced by the dopamine-1 receptor antagonist SCH 23390 but not by haloperidol

Life Sci.

(1989)

N.M. Bark

Heatstroke in psychiatric patients: two patients and a review

J. Clin. Psychiatry

(1982)

A.A. Borbély et al.

Phenothiazines

J.R. Coore

A fatal trip with ecstasy: a case of 3,4-methylene-dioxymethamphetamine/3,4-methylenedioxy-amphetamine toxicity

J. R. Soc. Med.

(1996)

S.M. Cordner et al.

Deaths of two hospital inpatients poisoned by pilocarpine

Br. Med. J.

(1986)

B. Cox et al.

Pharmacologic control of temperature regulation

Anna. Rev. Pharmacol.

(1977)

J. Delay et al.

Un neuroleptique majeur non-phénothiazinique et non-réserpinique, l'halopéridol dans le traitement des psychoses

Ann. Médico-Psychologiques

(1960)

FisherS. et al.

Cocaine and Biobehavioral Aspects

(1987)

S. Garattini et al.

Tricyclic antidepressant drugs

G. Garmany et al.

The use and action of chlorpromazine in psychoneuroses

Br. Med. J.

(1954)

D.J. Greenblatt et al.

Chlorpromazine and hyperpyrexia: a reminder that this drug affects the mechanisms which regulate body temperature

Clin. Pediatr.

(1973)

F.A. Gonzalez et al.

Physiological effects of cocaine in the squirrel monkey

Life Sci.

(1977)

Cited by (29)

Risk assessment for heat stress during work and leisure
2021, Toxicological Risk Assessment and Multi-System Health Impacts from Exposure
Rising environmental temperatures have become a growing challenge for societies across the globe. At the same time, occupational heat strain undermines the health and productivity of individuals working in key industries. In this chapter, we combine a narrative review with observational studies to outline the 18 factors affecting the risk for experiencing heat strain during work and leisure, which are: acclimatization, aging, anthropometrics, clothing, cultural habits, diet, disabilities, drugs and addictions, environmental stress, ethnicity, heat mitigation, medical conditions, metabolic demands, physical fitness, sex, sleep deprivation, work duration, and work experience. Addressing these risk factors will generate significant savings to healthcare systems from the occupational heat illness, absenteeism, and mortality associated with heat strain. Increased efforts should be made to educate individuals and organizations about the health, performance, and productivity risks related to heat strain and appropriate screening protocols should be incorporated within health and safety legislation.
Heat exhaustion
2018, Handbook of Clinical Neurology
Citation Excerpt :
However, many of the medications used to manage hypertension can modulate the heat loss responses of skin blood flow and sweating, thereby altering the body's physiologic capacity to dissipate heat during heat stress. For example, beta-blockers, diuretics, and vasodilators have been shown to reduce heat tolerance (Lomax and Schonbaum, 1998; Cheshire and Fealey, 2008), although the precise mechanisms of action have yet to be elucidated. Cardiovascular disease (e.g., coronary and valvular heart disease, chronic heart failure, cardiomyopathy, congenital heart defects, and cerebrovascular and peripheral vascular disease) may compromise thermoregulatory ability.
Heat exhaustion is part of a spectrum of heat-related illnesses that can affect all individuals, although children, older adults, and those with chronic disease are particularly vulnerable due to their impaired ability to dissipate heat. If left uninterrupted, there can be progression of symptoms to heatstroke, a life-threatening emergency. Signs and symptoms of heat exhaustion may develop suddenly or over time. Exposure to a hot environment for a prolonged period and performing exercise or work in the heat can overwhelm the body's ability to cool itself, causing heat exhaustion. Heat exhaustion can be worsened by dehydration due to inadequate access to water or insufficient fluid replacement. Heat exhaustion can be managed by the immediate reduction of heat gain by discontinuing exercise and reducing radiative heat source exposure. The individual should be encouraged to drink cool fluids and remove or loosen clothing to facilitate heat loss. In more extreme situations, more aggressive cooling strategies (e.g., cold shower, application of wet towels) to lower core temperature should be employed. Heat-related illnesses such as heat exhaustion can be prevented by increasing public awareness of the risks associated with exposure to high temperatures and prolonged exercise.
Heat-related deaths in Adelaide, South Australia: Review of the literature and case findings - An Australian perspective
2014, Journal of Forensic and Legal Medicine
Citation Excerpt :
Medications. Numerous medications may have side effects, which may impair survival in extreme heat conditions, classically these are the antipsychotic medications with anticholinergic side effects.54,61 Anticholinergics can decrease sweating and therefore heat dissipation.62
Heat waves are not uncommon in Australia, but the event of 2009 was particularly severe and ranks third of the 21 recorded heat wave events in south-eastern Australia in terms of the resulting mortality and morbidity. This is a review of Coronial autopsy findings in South Australia (which has an area of nearly 1 million square kilometres with a population of 1.6 million that predominantly resides within the region of the capital: Adelaide) during the period of the 2009 heat wave. Fifty-four post-mortem examinations were performed on cases in which exposure to high ambient temperature was regarded as having caused or significantly contributed to the death. The findings (including results of toxicological and biochemical analyses, where available) are reviewed and compared with the post-mortem examination findings in 22 deaths over the same period not attributed to the effects of heat. There were no specific autopsy findings that distinguished heat-related from non heat-related deaths. The lack of specific post-mortem findings increases the reliance on scene investigation in order to be able to categorise a death as being heat-related. A checklist for scene investigators is proposed in order to assist with collection of relevant data to assist the Coronial investigation process.
Heat Injury
2011, Pediatric Critical Care: Expert Consult Premium Edition
Heat Injury
2011, Pediatric Critical Care
Dopamine 2 antagonists suppress the jumping escape behavior of mice exposed to heat
2008, Journal of Thermal Biology
It is generally accepted that the dopamine system in the nucleus accumbens is activated and is involved in avoidance and escape behavior under aversive conditions. This study shows that the central dopamine system is involved in the jumping escape behavior in mice exposed to heat. In this study, the dopamine catabolite ratio in the nucleus accumbens was increased and dopamine 2 (D2) antagonists, chlorpromazine and haloperidol, inhibited the jumping escape behavior in mice exposed to 38.5 °C. Chlorpromazine increased hyperthermia in mice exposed to 38.5 °C, while haloperidol had no effect on rectal temperature in mice exposed to 38.5 °C. These results indicate that D2 antagonists inhibit the jumping escape behavior in mice exposed to heat and the inhibition mechanism of D2 antagonists is independent of the disturbance of autonomic thermoregulation.

View all citing articles on Scopus

View full text

Chapter 12 The effects of drugs on thermoregulation during exposure to hot environments

Publisher Summary

Lancet

Pharmacol. Biochem. Behav.

Pharmacol. Ther.

Neurosci. Behav. Rev.

Pharmacol. Biochem. Behav.

Pharmacol. Biochem. Behav.

Pharmacol. Ther.

Neuropharmacology

Pharmacol. Biochem. Behav.

Am. J. Med.

Pharmacol. Biochem. Behav.

Eur. J. Pharmacol.

Eur. J. Pharmacol.

Life Sci.

Heatstroke in psychiatric patients: two patients and a review

J. Clin. Psychiatry

Phenothiazines

A fatal trip with ecstasy: a case of 3,4-methylene-dioxymethamphetamine/3,4-methylenedioxy-amphetamine toxicity

J. R. Soc. Med.

Deaths of two hospital inpatients poisoned by pilocarpine

Br. Med. J.

Pharmacologic control of temperature regulation

Anna. Rev. Pharmacol.

Un neuroleptique majeur non-phénothiazinique et non-réserpinique, l'halopéridol dans le traitement des psychoses

Ann. Médico-Psychologiques

Cocaine and Biobehavioral Aspects

Tricyclic antidepressant drugs

The use and action of chlorpromazine in psychoneuroses

Br. Med. J.

Chlorpromazine and hyperpyrexia: a reminder that this drug affects the mechanisms which regulate body temperature

Clin. Pediatr.

Physiological effects of cocaine in the squirrel monkey

Life Sci.