Concentrations of soluble tumor necrosis factor and interleukin-6 receptors in heatstroke and heatstress

Hammami, Muhammad M.; Bouchama, Abderrezak; Al‐Sedairy, Sultan T.; Shail, Essam Al; AlOhaly, Yazid; Mohamed, Gamal

doi:10.1097/00003246-199708000-00017

Cited by 127 publications

(100 citation statements)

References 27 publications

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“…The plasma levels of TNF-a and IL-1b are shown to be well related to the severity of heatstroke (34,35). Indeed, increased levels of these cytokines are associated with heatstroke-induced arterial hypotension, cerebral ischemia, and neuronal damage (32,33; present results).…”

Section: Discussionsupporting

confidence: 63%

Prior Antagonism of Endothelin-1A Receptors Alleviates Circulatory Shock and Cerebral Ischemia During Rat Heatstroke

Liu¹,

Chen²,

Cheng³

et al. 2004

J Pharmacol Sci

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Abstract. In this study, we investigated the acute hemodynamic effects of an infusion of the endothelin-1 (ET-1)-A-selective receptor antagonists BQ-610 and BQ-123 in heatstroke rats with circulatory shock and cerebral ischemia. Heatstroke was induced by putting the anesthetized adult Sprague-Dawley rats into an ambient temperature of 42°C. The moment in which the mean arterial pressure dropped irreversibly from the peak for an extent of 25 mmHg was taken as the onset of heatstroke. The interval between initiation of heat exposure and heatstroke onset was found to be about 80 min for rats treated with vehicle solution. When the animals were exposed to 42°C for 80 min, hyperthermia, arterial hypotension, decrement of cardiac output (due to decreased stroke volume and decreased total peripheral resistance), increment of plasma ET-1 and tumor necrosis factor-a , and increment of cerebral ischemia and injury markers were manifested. Prior antagonism of ET-1 A receptors with BQ-610 (0.5 mg / kg, i.v.) or BQ-123 (1 mg / kg, i.v.), but not ET-1B receptors with BQ-788 (0.5 mg / kg, i.v.), 60 min before the initiation of heat exposure, appreciably alleviated hyperthermia, arterial hypotension, decreased cardiac output, increment of tumor necrosis factor-a , and increment of cerebral ischemia (e.g., glutamate and lactate / pyruvate ratio) and injury (e.g., glycerol) markers exhibited during heatstroke. The data indicates that ET-1A receptor antagonism may maintain appropriate levels of mean arterial pressure and cerebral circulation during heatstroke by reducing production of tumor necrosis factor-a .

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Section: Discussionsupporting

confidence: 63%

Prior Antagonism of Endothelin-1A Receptors Alleviates Circulatory Shock and Cerebral Ischemia During Rat Heatstroke

Liu¹,

Chen²,

Cheng³

et al. 2004

J Pharmacol Sci

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“…Intensive military training or strenuous exercise in the heat can lead to heatstroke, where an individual's core temperature can vary from approximately 41°C to 47°C during heat stroke [20][21][22]. Although our subjects averaged 37.9°C, no one topped 39.5°C or showed any signs of heat stroke.…”

Section: Discussionmentioning

confidence: 74%

Changes in Endothelial Markers during a Summer Ultra-Endurance Road Cycling Event in the Heat

BR¹

2016

Int J Sports Exerc Med

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Purpose: To assess the impact of completing a 164 km road cycling event performed in a hot environment (Wichita Falls, Texas in August), on endothelial biomarkers and resultant risk of blood clots in men and women.Methods: 37 event participants (28 men and 9 women; 51.8 ± 9.5 y) completed the ride. Plasma samples were collected in the morning before (PRE) and immediately after (IP) completing the ride. Concentrations of endothelial cell markers -endothelin-1 (ET-1), p-selectin, and intercellular adhesion molecule 1 (ICAM1), were measured and associations between changes from PRE-to IP-ride were examined as a function of race event completion time and participant characteristics (demographics and anthropometrics). Results:All of the endothelial cell markers (ET-1, p-selectin, and I-CAM1) increased significantly from PRE to IP. After controlling for PRE values, completion time was positively correlated with ET-1 (r = 0.42, p < 0.01) and negatively related to p-selectin (r = -0.42, p < 0.05). Waist circumference was positively related to ICAM1 (r = 0.34, p < 0.01). In addition, males had greater concentrations of ICAM1 (d = 1.32, p < 0.01) and p-selectin (d = 0.84, p < 0.05) than females. Conclusion:Completing a 164 km road cycling event in hot conditions resulted in increased concentrations of endothelial cell markers in men and women. Although this result may suggest endothelial cell injury, it is unclear whether this response is indicative of an increased risk of blood clot formation.

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“…During prolonged heat exposure, autonomic mechanisms of thermoregulatory control, such as sweating may become exhausted, resulting in dramatic increases in T c with values as high as ∼47°C reported in patients (Bouchama et al, 1991;1993;Chang, 1993;Hammami et al, 1997;Hashim et al, 1997;Lu et al, 2004;Sonna et al, 2004). Hypothermia (∼ 7°C below baseline) and fever (∼ 1-2°C above baseline) are long-term heat stroke recovery responses that are less well-recognized, but are thought to be a consequence of the systemic inflammatory response (SIRS) that occurs in response to endotoxin leakage from the ischemic GI tract (Attia et al, 1983;Austin and Berry, 1956;Leon et al, 2005;Malamud et al, 1946;Romanovsky and Blatteis, 1996;Wilkinson et al, 1988;Wright, 1976).…”

Section: Physiological Responses To Heat Stressmentioning

confidence: 99%

Thermoregulatory responses to environmental toxicants: The interaction of thermal stress and toxicant exposure

Leon

2008

Toxicology and Applied Pharmacology

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Concentrations of soluble tumor necrosis factor and interleukin-6 receptors in heatstroke and heatstress

Cited by 127 publications

References 27 publications

Prior Antagonism of Endothelin-1A Receptors Alleviates Circulatory Shock and Cerebral Ischemia During Rat Heatstroke

Prior Antagonism of Endothelin-1A Receptors Alleviates Circulatory Shock and Cerebral Ischemia During Rat Heatstroke

Changes in Endothelial Markers during a Summer Ultra-Endurance Road Cycling Event in the Heat

Thermoregulatory responses to environmental toxicants: The interaction of thermal stress and toxicant exposure

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