The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage

Lee, Joshua F.; Harrison, Michelle; Brown, Skyler

doi:10.1152/japplphysiol.00878.2012

Cited by 13 publications

(19 citation statements)

References 46 publications

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“…For example, during a heat stress that increases internal temperature 0.5 to ~1.2°C, mean cerebral perfusion either does not change, or only modestly decreases (137,141,264,265). In contrast, up to 20% to 30% reductions in mean cerebral perfusion are observed when internal temperature is elevated 1.5°C or more (65,68,127,174,210). Based upon these observations, the magnitude of the reduction in cerebral perfusion seems to be related, in a graded manner, to the extent of the heat stress; though the specifics of this response, such as the threshold, “gain,” and saturation points remain uninvestigated.…”

Section: Heat Stress and The Cerebral Circulationmentioning

confidence: 91%

Human Cardiovascular Responses to Passive Heat Stress

Crandall

Wilson

2014

Comprehensive Physiology

149

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 The Cerebral Circulationmentioning

confidence: 91%

Human Cardiovascular Responses to Passive Heat Stress

Crandall

Wilson

2014

Comprehensive Physiology

149

136

View full text Add to dashboard Cite

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“…Cerebral responses to rebreathing were assessed using MCA V mean as well as CVCi, which takes into consideration rebreathing induced changes in arterial pressure. MCA V mean and CVCi were analyzed as absolute values and as percent changes to account for reductions in baseline that occur during heat stress [3, 15, 29]. …”

Section: Methodsmentioning

confidence: 99%

“…Whole body heat stress increases sympathetic outflow [12] and reduces cerebral perfusion [3, 15, 29], and if heat stress mediated elevations in SNA are directed to the cerebral circulation, it is plausible that the capacity for cerebral vasodilation might be diminished during a rebreathing task in this thermal condition. This is an important question given the already reduced cerebral perfusion in this thermal state [3, 15, 29].…”

Section: Introductionmentioning

confidence: 99%

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Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

et al. 2014

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Objective Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP). Methods Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS+20 mmHg LBNP (HSLBNP) while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA Vmean). Cerebrovascular responses were calculated from the slope of the change in MCA Vmean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide (PETCO2) during rebreathing. Results MCA Vmean was similar in HS (55±19 cm·s−1) and HSLBNP (52±16 cm·s−1), and both values were reduced relative to NT (66±20 cm·s−1), yet the rise in MCA Vmean per Torr increase in PETCO2 during rebreathing was similar in each condition (NT: 2.5±0.6 cm/s·Torr−1; HS: 2.4±0.8 cm/s·Torr−1; HSLBNP: 2.1±1.1 cm/s·Torr−1). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1±0.65 cm/s/mmHg·100·Torr−1; HS: 2.4±0.8 cm/s/mmHg·100·Torr−1; HSLBNP: 2.0±1.0 cm/s/mmHg·100·Torr−1). Interpretations These data indicate that cerebrovascular reactivity is not compromised during whole body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.

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“…simulated hemorrhage challenges while in this thermal condition (1,13,18,20,21,37,38). The mechanisms causing these responses are likely multifactorial, but could be related in part to compromised cardiac function.…”

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confidence: 99%

Beneficial effects of elevating cardiac preload on left-ventricular diastolic function and volume during heat stress: implications toward tolerance during a hemorrhagic insult

Pecini

Dalsgaard

Bundgaard‐Nielsen

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Volume loading normalizes tolerance to a simulated hemorrhagic challenge in heat-stressed individuals, relative to when these individuals are thermoneutral. The mechanism(s) by which this occurs is unknown. This project tested two unique hypotheses; that is, the elevation of central blood volume via volume loading while heat stressed would 1) increase indices of left ventricular diastolic function, and 2) preserve left ventricular end-diastolic volume (LVEDV) during a subsequent simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Indices of left ventricular diastolic function were evaluated in nine subjects during the following conditions: thermoneutral, heat stress, and heat stress after acute volume loading sufficient to return ventricular filling pressures toward thermoneutral levels. LVEDV was also measured in these subjects during the aforementioned conditions prior to and during a simulated hemorrhagic challenge. Heat stress did not change indices of diastolic function. Subsequent volume infusion elevated indices of diastolic function, specifically early diastolic mitral annular tissue velocity (E') and early diastolic propagation velocity (E) relative to both thermoneutral and heat stress conditions (P < 0.05 for both). Heat stress reduced LVEDV (P < 0.05), while volume infusion returned LVEDV to thermoneutral levels. The reduction in LVEDV to LBNP was similar between thermoneutral and heat stress conditions, whereas the reduction after volume infusion was attenuated relative to both conditions (P < 0.05). Absolute LVEDV during LBNP after volume loading was appreciably greater relative to the same level of LBNP during heat stress alone. Thus, rapid volume infusion during heat stress increased indices of left ventricular diastolic function and attenuated the reduction in LVEDV during LBNP, both of which may serve as mechanisms by which volume loading improves tolerance to a combined hyperthermic and hemorrhagic challenge.

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The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage

Cited by 13 publications

References 46 publications

Human Cardiovascular Responses to Passive Heat Stress

Human Cardiovascular Responses to Passive Heat Stress

Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

Beneficial effects of elevating cardiac preload on left-ventricular diastolic function and volume during heat stress: implications toward tolerance during a hemorrhagic insult

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