Effect of temperature on cutaneous venomotor reflexes in man.

Zitnik, Ralph S.; Ambrosioni, Ettore; Shepherd, JT

doi:10.1152/jappl.1971.31.4.507

Cited by 36 publications

(11 citation statements)

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“…Consistent with this hypothesis, cutaneous vasoconstrictor responsiveness to exogenous and endogenous vasoconstrictor stimuli are attenuated during both whole-body and local heating (186,262). These findings are consistent with the effects of local and whole-body heating on constrictor responses in isolated hand veins (282). Subsequent studies revealed that substances released during heat stress, such as nitric oxide and/or vasoactive peptide(s), may directly attenuate cutaneous adrenergic vasoconstrictor responsiveness for a given neural signal (136,239–241).…”

Section: Heat Stress and Human Baroreflex Responsivenesssupporting

confidence: 90%

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Human Cardiovascular Responses to Passive Heat Stress

Crandall

Wilson

2014

Comprehensive Physiology

153

136

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Heat stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially vulnerable to the stress imposed on the cardiovascular system during exposure to hot ambient conditions. This review focuses on the cardiovascular responses to heat stress that are necessary for heat dissipation. To accomplish this regulatory feat requires complex autonomic nervous system control of the heart and various vascular beds. For example, during heat stress cardiac output increases up to twofold, by increases in heart rate and an active maintenance of stroke volume via increases in inotropy in the presence of decreases in cardiac preload. Baroreflexes retain the ability to regulate blood pressure in many, but not all, heat stress conditions. Central hypovolemia is another cardiovascular challenge brought about by heat stress, which if added to a subsequent central volumetric stress, such as hemorrhage, can be problematic and potentially dangerous, as syncope and cardiovascular collapse may ensue. These combined stresses can compromise blood flow and oxygenation to important tissues such as the brain. It is notable that this compromised condition can occur at cardiac outputs that are adequate during normothermic conditions but are inadequate in heat because of the increased systemic vascular conductance associated with cutaneous vasodilation. Understanding the mechanisms within this complex regulatory system will allow for the development of treatment recommendations and countermeasures to reduce risks during the ever-increasing frequency of severe heat events that are predicted to occur.

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Section: Heat Stress and Human Baroreflex Responsivenesssupporting

confidence: 90%

“…14). Such a finding is not surprising given changes in venous properties (i.e., increased capacitance and decreased responsiveness to adrenergic agents) with elevated tissue temperature (83,84,214,253,282). …”

Section: Heat Stress and Tolerance To A Hypotensive Challengementioning

confidence: 92%

Human Cardiovascular Responses to Passive Heat Stress

Crandall

Wilson

2014

Comprehensive Physiology

153

136

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“…However, the greater insulin absorption rate during exercise in warm temperature compared with the resting state in the same temperature cannot be explained by the same mechanism, because skin temperature fell during exercise at 30°C. This is consistent with the previous finding that constriction of skin veins and decrease in skin blood flow occurs during exercise in warm temperature (19). A likely explanation for the enhanced insulin absorption in warm temperature during exercise is that repetitious muscle contractions result in a massagelike effect, which enhances insulin absorption from subcutaneous tissue (3).…”

Section: Discussionsupporting

confidence: 92%

Combined Effect of Exercise and Ambient Temperature on Insulin Absorption and Postprandial Glycemia in Type I Patients

Rönnemaa

Koivisto

1988

Diabetes Care

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We studied the combined effect of cool (10 degrees C) and warm (30 degrees C) ambient temperatures and physical exercise on insulin absorption and postprandial glycemia. Nine type I (insulin-dependent) diabetic patients were injected subcutaneously with their usual morning dose of short- and intermediate-acting human insulin and were given breakfast. Warm temperature was associated with 3- to 5-fold higher insulin absorption (P less than .01) and significantly lower blood glucose concentration (P less than .001) than cool temperature regardless of exercise. Exercise was associated with 28% (P less than .01) and 22% (P less than .05) increases in plasma insulin and maximally 5.7 mM (P less than .025) and 7.1 mM (P less than .01) lower blood glucose at cool and warm temperatures, respectively. Warm temperature and exercise had an additive effect in stimulating insulin absorption and in lowering blood glucose concentrations. However, there was no evidence of synergism between higher temperature and exercise in increasing free-insulin concentrations or decreasing blood glucose concentrations. To avoid postprandial hyperglycemia at cool temperature or hypoglycemia after exercise at warm temperature, appropriate adjustments in diet and insulin dose, or both, should be made.

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“…With regard to the observed hysteresis in the immediate recovery period, several studies have demonstrated the preservation of baroreflex control of HR during heat stress (8,11,38,40,41). Interestingly, although vascular sympathetic nerve activity is increased during heat stress (12), heat-induced attenuation of postsynaptic vasoconstrictor responsiveness results in progressive and profound reductions in MAP (14) in rats (20,26,28) and humans (11,14,39,42). Kregel et al (20,26,27) demonstrated reduced vascular reactivity during exposure to high local temperatures in the rat mesenteric arteries, both in vivo and in isolated vessel preparations.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular and thermoregulatory dysregulation over 24 h following acute heat stress in rats

Quinn

Audet

Charkoudian

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Quinn CM, Audet GN, Charkoudian N, Leon LR. Cardiovascular and thermoregulatory dysregulation over 24 h following acute heat stress in rats. Am J Physiol Heart Circ Physiol 309: H557-H564, 2015. First published June 12, 2015; doi:10.1152/ajpheart.00918.2014.-The influences of severe heat stroke (HS) on cardiovascular function during recovery are incompletely understood. We hypothesized that HS would elicit a heart rate (HR) increase persisting through 24 h of recovery due to hemodynamic, thermoregulatory, and inflammatory events, necessitating tachycardia to support mean arterial pressure (MAP). Core temperature (Tc), HR, and MAP were measured via radiotelemetry in conscious male Fischer 344 rats (n ϭ 22; 282.4 Ϯ 3.5 g) during exposure to 37°C ambient temperature until a maximum Tc of 42.0°C, and during recovery at 20°C ambient temperature through 24 h. Rats were divided into Mild, Moderate, and Severe groups based on pathophysiology. HS rats exhibited hysteresis relative to Tc with HR higher for a given Tc during recovery compared with heating (P Ͻ 0.0001). "Reverse" hysteresis occurred in MAP with pressure during cooling lower than heating per degree Tc (P Ͻ 0.0001). Mild HS rats showed tachycardia [P Ͻ 0.01 vs. control (Con)] through 8 h of recovery, elevated MAP (P Ͻ 0.05 vs. Con) for the initial 5 h of recovery, with sustained hyperthermia (P Ͻ 0.05 vs. Con) through 24 h. Moderate HS rats showed significant tachycardia (P Ͻ 0.01 vs. Con), normal MAP (P Ͼ 0.05 vs. Con), and rebound hyperthermia from 4 to 24 h post-HS (P Ͻ 0.05 vs. Con). Severe HS rats showed tachycardia (P Ͻ 0.05 vs. Con), hypotension (P Ͻ 0.01 vs. Con), and hypothermia for 24 h (P Ͻ 0.05 vs. Con). Severe HS rats showed 14-and 12-fold increase in heart and liver inducible nitric oxide synthase expression, respectively. Hypotension and hypothermia in Severe HS rats was consistent with inducible nitric oxide synthasemediated systemic vasodilation. These findings provide mechanistic insight into hemodynamic and thermoregulatory impairments during 24 h of HS recovery. thermoregulation; heart rate; heat stroke; autonomic nervous system; blood pressure; iNOS NEW & NOTEWORTHYThe present study provides mechanistic insight into hemodynamic and thermoregulatory impairments during 24 h of heat stroke recovery. These findings are qualitatively similar to clinical manifestations observed in heat stroke patients and provide further insight into multiple stressors placed on integrative cardiovascular regulation during the 24 h following severe heat stress.HEAT STROKE (HS) IS A DEBILITATING illness characterized by myriad thermoregulatory, cardiovascular, and systemic inflammatory abnormalities. Sustained exposure to uncompensable heat stress results in HS, which manifests as profound autonomic and thermoregulatory dysfunction, often complicated by coagulopathies and precipitating catastrophic multiorgan failure.In response to whole body hyperthermia in humans and rats, heart rate (HR) increases linearly with increasing core temperature (T c ) (21,30). This...

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Effect of temperature on cutaneous venomotor reflexes in man.

Cited by 36 publications

References 0 publications

Human Cardiovascular Responses to Passive Heat Stress

Human Cardiovascular Responses to Passive Heat Stress

Combined Effect of Exercise and Ambient Temperature on Insulin Absorption and Postprandial Glycemia in Type I Patients

Cardiovascular and thermoregulatory dysregulation over 24 h following acute heat stress in rats

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