Cardiovascular changes during syncope induced by tilting men in the heat.

Lind, A. R.; Leithead, C.S.; McNicol, G. W.

doi:10.1152/jappl.1968.25.3.268

Cited by 113 publications

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“…Previous studies showed that humans become more susceptible to fainting during orthostatic stress and gravitation acceleration when combined with heat stress (1,15). Lind et al (15) suggested that reductions in orthostatic tolerance in heated humans were not a result of vascular pooling.…”

Section: Perspectivesmentioning

confidence: 98%

“…Lind et al (15) suggested that reductions in orthostatic tolerance in heated humans were not a result of vascular pooling. Thus a reasonable hypothesis leading to reduced tolerance to orthostatic stress would be heat-induced alterations in baroreflex control of blood pressure and heart rate.…”

Section: Perspectivesmentioning

confidence: 99%

“…Moreover, we recently reported that carotid baroreflex regulation of arterial blood pressure is impaired following whole body heating (2). Thus it remains a possibility that although baroreflex control of MSNA is not affected by elevations in internal temperature, altered postsynaptic responses may contribute to reduced tolerance to orthostatic stress observed in heat-stressed humans (1,15).…”

Section: Perspectivesmentioning

confidence: 99%

“…DURING EXPOSURE TO INCREASED thermal load, humans become more susceptible to syncope during orthostatic or gravitational acceleration (1,15). Baroreflexes are important in the regulation of blood pressure, but relatively little is known about the effects of whole body heating on baroreflex regulation.…”

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confidence: 99%

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Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

Cui

Wilson

Crandall

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans. Am J Physiol Regulatory Integrative Comp Physiol 282: R252-R258, 2002; 10.1152/ajpregu. 00337.2001.-To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature (P Ͻ 0.01), MSNA (P Ͻ 0.01), heart rate (P Ͻ 0.01), and skin blood flow (P Ͻ 0.001), whereas mean arterial blood pressure did not change significantly (P Ͼ 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (Ϫ128.3 Ϯ 13.9 U ⅐ beats Ϫ1 ⅐ mmHg Ϫ1 ) was similar (P ϭ 0.31) with normothermia (Ϫ140.6 Ϯ 21.1 U ⅐ beats Ϫ1 ⅐ mmHg Ϫ1 ). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating. baroreflex sensitivity; muscle sympathetic nerve activity; heart rate; heat stress DURING EXPOSURE TO INCREASED thermal load, humans become more susceptible to syncope during orthostatic or gravitational acceleration (1, 15). Baroreflexes are important in the regulation of blood pressure, but relatively little is known about the effects of whole body heating on baroreflex regulation. Previous studies revealed that electrical stimulation of the hypothalamus, which is the central neural structure governing thermoregulation (9, 20), modifies the baroreceptor reflex. Therefore, it is possible that whole body heating impairs baroreflex control of blood pressure, thereby contributing to the reduction in orthostatic tolerance during exposure to hyperthermic environmental conditions.Although the effects of whole body heating on baroreflex function have not been fully identified, during heat stress, baroreflexes remain capable of modulating efferent sympathetic nerve activity as evidenced by the observation that increases in blood pressure via phenylephrine HCl infusion decrease muscle sympathetic nerve activity (MSNA) in heat-stressed humans (3). Similar changes in splanchnic sympathetic nerve activity have been reported during blood pressure perturbations in hyperthermic rats (18).Previously, studies investigated the effects of heat stress on baroreflex function in rats (18, 22) and baboons (10). With the use of different techniques, these investigators concluded that hyperthermic exposu...

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Section: Perspectivesmentioning

confidence: 98%

Section: Perspectivesmentioning

confidence: 99%

Section: Perspectivesmentioning

confidence: 99%

mentioning

confidence: 99%

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Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

Cui

Wilson

Crandall

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38).…”

mentioning

confidence: 99%

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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CG. Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress. J Appl Physiol 104: 976-981, 2008. First published January 24, 2008 doi:10.1152/japplphysiol.01040.2007.-This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO 2 ). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO 2 ϳ20 Torr) and normoxic hypercapnic (increase in PETCO 2 ϳ9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and PETCO 2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (1.1 Ϯ 0.2°C, P Ͻ 0.001) and reduced middle cerebral artery blood velocity by 8 Ϯ 8 cm/s (P ϭ 0.01), reduced CBVC by 0.09 Ϯ 0.09 CBVC units (P ϭ 0.02), and decreased PETCO 2 by 3 Ϯ 4 Torr (P ϭ 0.07), while mean arterial blood pressure was well maintained (P ϭ 0.36). The slope of the CBVC-PET CO 2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 Ϯ 0.006 vs. 0.009 Ϯ 0.004 CBVC units/Torr, P ϭ 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PETCO 2 relationship was not different between normothermia and heat stress conditions (0.028 Ϯ 0.020 vs. 0.023 Ϯ 0.008 CBVC units/Torr, P ϭ 0.31). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16, 36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41). Decreased cerebral perfusion would theoretically reduce the functional reserve by which cerebral blood flow can decrease further, before the onset of syncopal symptoms.It is unlikely that the relatively small decrease in PET CO 2 (i.e., ϳ2 Torr) in response to passive heat stress is the sole mechanism leading to the observed reduction in cerebral perfusion. However, this assumption is based on ca...

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Cutaneous Vasodilator and Vasoconstrictor Mechanisms in Temperature Regulation

Johnson

Minson

Kellogg

2014

Comprehensive Physiology

330

290

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In this review, we focus on significant developments in our understanding of the mechanisms that control the cutaneous vasculature in humans, with emphasis on the literature of the last half-century. To provide a background for subsequent sections, we review methods of measurement and techniques of importance in elucidating control mechanisms for studying skin blood flow. In addition, the anatomy of the skin relevant to its thermoregulatory function is outlined. The mechanisms by which sympathetic nerves mediate cutaneous active vasodilation during whole body heating and cutaneous vasoconstriction during whole body cooling are reviewed, including discussions of mechanisms involving cotransmission, NO, and other effectors. Current concepts for the mechanisms that effect local cutaneous vascular responses to local skin warming and cooling are examined, including the roles of temperature sensitive afferent neurons as well as NO and other mediators. Factors that can modulate control mechanisms of the cutaneous vasculature, such as gender, aging, and clinical conditions, are discussed, as are nonthermoregulatory reflex modifiers of thermoregulatory cutaneous vascular responses.

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Cardiovascular changes during syncope induced by tilting men in the heat.

Cited by 113 publications

References 0 publications

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Cutaneous Vasodilator and Vasoconstrictor Mechanisms in Temperature Regulation

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