Thermal regulatory dysfunction of growth hormone in classical heat stroke?

1996 ◽  
Vol 134 (6) ◽  
pp. 727-730
Author(s):  
Abdulaziz Alzeer ◽  
Abdullah Al Arifi ◽  
Mohsen El-Hazmi ◽  
Arjumand S Warsy ◽  
Eric S Nylen

Alzeer A, Al Arifi A, El-Hazmi M, Warsy AS, Nylen ES. Thermal regulatory dysfunction of growth hormone in classical heat stroke? Eur J Endocrinol 1996;134:727–30. ISSN 0804–4643 Growth hormone (GH) secretion associated with classical (non-exertional) heat stroke (HS) was evaluated in 26 HS victims and 10 control (non heat-exhausted) subjects during the annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, the GH level was 1.54 ± 0.14 ng/ml (approximately 3.5-fold higher in the HS victims compared to controls; p = 0.005). The GH levels subsequently declined by 78% by 24 h. The categorized GH response was significantly associated with survival for those subjects with a GH level of < 5.53 ng/ml by 6 h (chi-squared test; p = 0.06). In those patients who died (N = 6), there was a continued increase in GH levels from the time of admission, which peaked at 6 h. In those patients who survived, the GH levels peaked at the time of admission and declined rapidly thereafter. There was a direct correlation of age and GH level upon admission (p = 0.02), as well as to peak GH (p = 0.041). However, there was no relationship of GH level to either body core temperature or the cooling time. In summary, HS induced significant GH secretion. The degree of GH response was not related to the body core temperature and was more pronounced in older individuals and in those that died. Although patients with GH deficiency and HS are characterized by anhidrosis/hypohidrosis, there does not appear to be dysfunction of GH response to heat stress-associated HS. In contrast, a vigorous GH response at 6 h suggested a worse outcome. ES Nylen, Rm GE 246, VAMC, 50 Irving St, NW Washington, DC 20422, USA

2017 ◽  
Vol 122 (4) ◽  
pp. 933-944 ◽  
Author(s):  
Glen P. Kenny ◽  
Ryan McGinn

Performing exercise, especially in hot conditions, can heat the body, causing significant increases in internal body temperature. To offset this increase, powerful and highly developed autonomic thermoregulatory responses (i.e., skin blood flow and sweating) are activated to enhance whole body heat loss; a response mediated by temperature-sensitive receptors in both the skin and the internal core regions of the body. Independent of thermal control of heat loss, nonthermal factors can have profound consequences on the body’s ability to dissipate heat during exercise. These include the activation of the body’s sensory receptors (i.e., baroreceptors, metaboreceptors, mechanoreceptors, etc.) as well as phenotypic factors such as age, sex, acclimation, fitness, and chronic diseases (e.g., diabetes). The influence of these factors extends into recovery such that marked impairments in thermoregulatory function occur, leading to prolonged and sustained elevations in body core temperature. Irrespective of the level of hyperthermia, there is a time-dependent suppression of the body’s physiological ability to dissipate heat. This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifest most commonly as postexercise hypotension. This review examines the current knowledge regarding the restoration of thermoregulation postexercise. In addition, the factors that are thought to accelerate or delay the return of body core temperature to resting levels are highlighted with a particular emphasis on strategies to manage heat stress in athletic and/or occupational settings.


2019 ◽  
Vol 127 (5) ◽  
pp. 1338-1348 ◽  
Author(s):  
Orlando Laitano ◽  
Lisa R. Leon ◽  
William O. Roberts ◽  
Michael N. Sawka

During the past several decades, the incidence of exertional heat stroke (EHS) has increased dramatically. Despite an improved understanding of this syndrome, numerous controversies still exist within the scientific and health professions regarding diagnosis, pathophysiology, risk factors, treatment, and return to physical activity. This review examines the following eight controversies: 1) reliance on core temperature for diagnosing and assessing severity of EHS; 2) hypothalamic damage induces heat stroke and this mediates “thermoregulatory failure” during the immediate recovery period; 3) EHS is a predictable condition primarily resulting from overwhelming heat stress; 4) heat-induced endotoxemia mediates systemic inflammatory response syndrome in all EHS cases; 5) nonsteroidal anti-inflammatory drugs for EHS prevention; 6) EHS shares similar mechanisms with malignant hyperthermia; 7) cooling to a specific body core temperature during treatment for EHS; and 8) return to physical activity based on physiological responses to a single-exercise heat tolerance test. In this review, we present and discuss the origins and the evidence for each controversy and propose next steps to resolve the misconception.


Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 41-44 ◽  
Author(s):  
M Cabanac

The mammalian brain has poor tolerance to increased temperature. However, when body core temperature rises during exercise or heat stress, the temperature of the brain can remain at a lower level, somewhat independent of the rest of the body. In several mammals the cooling of the brain is related to anatomically well-defined countercurrent heat exchangers. Humans lack these distinct anatomic structures, but significant cooling of the brain can nevertheless occur. Such selective cooling of the brain may have important medical implicantions.


1979 ◽  
Vol 46 (5) ◽  
pp. 978-983 ◽  
Author(s):  
J. B. Mercer ◽  
C. Jessen

Investigations were carried out to determine whether a nonthermal input is involved in the control of respiratory evaporative heat loss (REHL) in exercising goats. Two goats were implanted with hypothalamic perfusion thermodes and three goats were implanted with intravascular heat exchangers to clamp hypothalamic temperature and total body core temperature, respectively. At 30 degrees C air temperature REHL was measured while the animals were resting or walking on a treadmill (3 km.h-1, 5 degrees gradient). When the hypothalamic temperature was clamped between 33.0 and 43.0 degrees C the slopes of the responses relating increased REHL to hypothalamic temperature were similar during rest and exercise. However, the threshold hypothalamic temperatures for the increased REHL responses were lower during exercise than at rest, presumably due to higher extrahypothalamic temperatures. When the body core temperature was clamped between 37.0 and 40.4 degrees C the slopes of the responses relating increased REHL to total body core temperature during exercise showed only minor differences compared to those at rest, none of them conclusively indicating nonthermal influences.


Rangifer ◽  
1985 ◽  
Vol 5 (1) ◽  
pp. 10 ◽  
Author(s):  
James B. Mercer ◽  
Helge K. Johnsen ◽  
Svein D. Mathiesen ◽  
Arnoldus Schytte Blix

<p>A method is described whereby it is possible to alter total body core temperature independently of environmetal temperature and/or exercise in conscious reindeer. The method employs the use of a simple heat exchanger introduced through a permanent rumen fistula. The heat exchanger consists of a 7 m long coil of flexible plastic tubing (OD, 10.0 mm, ID, 8.0 mm). By perfusing the tubing with thermostatically controlled water, heat can be added to or subtracted from the body core at rates equalling several times resting heat production. It is suggested that the method could be used in any large ruminant species.</p><p>En intra-rumenal varmeveksler til bruk i st&oslash;rre, uanesteserte dyr.</p><p>Abstract in Norwegian / Sammendrag: Vi har i denne unders&oslash;kelsen beskrevet en metode for hvordan kroppstemperatur hos uanesteserte reinsdyr kan endres uavhengig av omgivelsestemperatur og om dyret l&oslash;per eller ikke. Metoden inneb&aelig;rer bruk av en enkel varmeveksler som plasseres i dyrets vom gjennom en permanent vom-fistel. Varmeveksleren best&aring;r av en 7 m lang kveil av fleksibel plastslange (ytre diameter 10.0 mm, indre diameter 8.0 mm). Ved &aring; perfundere slangen med vann av en bestemt temperatur er det mulig &aring; fjerne eller tilf&oslash;re kroppen en varmemengde som tilsvarer flere ganger dyrets varmeproduksjon. Vi mener at denne metoden kan tilpasses alle store dr&oslash;vtyggere.</p><p>Potsiin asetettavan l&aring;mpotilan muuttajan k&aring;ytto suurilla nukkumattomilla el&aring;imill&aring;.</p><p>Abstract in Finnish / Yhteenveto: Tutkimuksessa olemme kuvanneet menetelman, jolla voidaan muuttaa nukuttamattoman poron ruumiinl&aring;mpotilaa riippumatta ulkolampotilasta tai siita juokseeko el&aring;in vai ei. Menetelmassa k&aring;ytaan yksinkertaista l&aring;mpotilan muuttajaa, joka asetetaan elaimeen pysyyan potsifistulan kautta. L&aring;mpotilan muuttaja kasitt&aring;a 7 m pitkan muoviletkurullan (letkun halkaisija 10.6 mm, reian halkaisija" 8.0 mmJTTaytt&aring;m&aring;lla letku tietyn lampoisell&aring; vedella on mahdollista joko laskea tai nostaa ruumiin lampom&aring;&aring;r&aring;a niin, etta se vastaa moninkertaisesti elaimen omaa l&aring;mmontuottoa. Oletamme, etta menetelm&aring;a voidaan kaytta&aring; kaikille suurille m&aring;rehtijoille.</p>


1997 ◽  
Vol 82 (5) ◽  
pp. 1406-1410 ◽  
Author(s):  
James E. Fewell ◽  
Patricia A. Tang

Fewell, James E., and Patricia A. Tang. Pregnancy alters body-core temperature response to a simulated open field in rats. J. Appl. Physiol. 82(4): 1406–1410, 1997.—Exposure of a rat to a novel environment (e.g., a simulated open field) induces a transient increase in body-core temperature, which is often called stress-induced hyperthermia. Although pregnancy is known to influence thermoregulatory control, its effect on stress-induced hyperthermia is unknown. Therefore, 24 Sprague-Dawley rats (8 nonpregnant and 16 pregnant) were studied to test the hypothesis that pregnancy would alter the development of stress-induced hyperthermia after exposure to a simulated open field. Body-core temperature index increased significantly after exposure to a simulated open field in nonpregnant and gestation day-10 rats but not in gestation day-15 and day-20 rats. Thus our data provide evidence that pregnancy influences the body-core temperature response of rats exposed to a simulated open field in a gestation-dependent fashion. The functional consequences as well as the mechanisms involved remain to be determined.


2013 ◽  
Vol 1 (1) ◽  
pp. 135-139
Author(s):  
Metodija Kjertakov ◽  
Yoram Epstein

Exercising in hot and especially humid environment can cause rise in body core temperature to such a critical level that it does not only reduce performance, but also may ultimately lead to exertional heat stroke (EHS). This illness is true medical emergency that can result in significant morbidity and mortality, if not early recognized and promptly treated. Diagnostic criteria for EHS are body core temperature above 40ºC and central nerve system dysfunction. Any athlete experiencing such symptoms should be immediately exposed to aggressive cooling treatment aimed to lower the elevated core temperature to near normal as quickly as possible. Ice water immersion is highly recommended as a cooling method because it provides the fastest cooling rates and is associated with lowest mortality rates. Athletes cooled rapidly soon after the onset of EHS usually recover without complications and are able to return to normal training in hot environment within a few weeks. EHS is also a preventable condition, and its occurrence can be minimized by implementing a few simple measures.


Author(s):  
Oleg Vesnovsky ◽  
Yiyong Li ◽  
L. D. Timmie Topoleski ◽  
Liang Zhu

In recent years, outbreaks of highly contagious diseases, like the Ebola virus, have motivated vigorous efforts to screen travelers entering the United States, especially at airports. Screening involves monitoring the body temperature of entering travelers, and blocking entry of those showing a fever, indicating a potential infection. Typically, screening is performed using commercially available non-contact infrared thermometers (NCITs). These thermometers require specific use protocols (e.g., working distances) to provide accurate results, which may not be followed by inspectors reluctant to approach potentially contagious travelers. Furthermore, the NCITs’ accuracy is based on an assumption that the NCIT readings from a forehead will predict the body core temperatures using a simple common one-size-fits-all correction offset. Unfortunately, the temperature detected on the forehead surface by an NCIT may not represent the true body core temperature, due to the changing conditions of the external environment and/or surface conditions of the forehead skin. It is not clear whether the correction factor is able to adjust to the thermal environment, or whether the surface condition of the forehead, including sweat and skin tone, affects the NCIT readings. Before a clinical study is conducted to understand the differences between the forehead temperatures and the body core temperatures, a computational model to simulate temperature distribution inside and on the surface of the body is a cost-effective way to identify factors that influence the temperatures and to study the reasons for their deviations. The objectives of this study were to 1) develop a numerical whole-body model and perform computational heat transfer simulations of different body geometries and 2) perform parametric studies to evaluate the effect of environmental factors, such as air temperature and heat transfer coefficient, on the differences between the forehead temperature and body core temperature. This data can be used to evaluate correction factors or needed to use the measured forehead temperature to predict the body core temperature.


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