Selective brain cooling in hyperthermia: the mechanisms and medical implications

Nagasaka, Tetsuo; Brinnel, H.; Hales, J. R. S.; Ogawa, Tokuo

doi:10.1016/s0306-9877(98)90019-6

Cited by 41 publications

(20 citation statements)

References 21 publications

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“…Despite a reliance on sweating as a means of heat loss, the body water status of zebras may not ever be seriously compromised. The argument that horses, which like donkeys have penetrated arid areas, particularly after domestication, avoid hyperthermia by relying on selective brain cooling and a high capacity for sweating (Nagasaka et al 1998) is clearly incompatible with our data and our concept of selective brain cooling. So too is the view, still held by a few in the face of mounting evidence to the contrary, that selective brain cooling is an adaptive mechanism to protect the brain from thermal damage (Brinnel et al 1987;Nagasaka et al 1998).…”

Section: Discussioncontrasting

confidence: 68%

“…The argument that horses, which like donkeys have penetrated arid areas, particularly after domestication, avoid hyperthermia by relying on selective brain cooling and a high capacity for sweating (Nagasaka et al 1998) is clearly incompatible with our data and our concept of selective brain cooling. So too is the view, still held by a few in the face of mounting evidence to the contrary, that selective brain cooling is an adaptive mechanism to protect the brain from thermal damage (Brinnel et al 1987;Nagasaka et al 1998). McConaghy and colleagues (1995) argue that 'it is difficult to imagine any purpose for the cooling of the cavernous sinus other than to cool the brain during systemic hyperthermia', even though, for one horse for which the data are shown, the magnitude of selective brain cooling remained constant at •0.3°C as blood temperature increased from 38 to 41°C.…”

Section: Discussioncontrasting

confidence: 68%

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Absence of Selective Brain Cooling in Free‐Ranging Zebras in Their Natural Habitat

Fuller

Maloney

Kamerman

et al. 2000

Experimental Physiology

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We used implanted miniature data loggers to measure brain and arterial blood temperatures in three freeranging zebras (Equus burchelli) in their natural habitat, every 5 min for 9 days. The animals experienced globe temperatures exceeding 40°C, and radiant heat load of about 1000 W m¦Â. Arterial blood exhibited a moderate amplitude (1.7°C) nychthemeral rhythm, with an acrophase at •19.00 h and a nadir late in the morning, at •10.00 h. Brain temperature consistently exceeded blood temperature, on average by 0.2-0.4°C, and changes in brain temperature closely tracked changes in blood temperature. There was no evidence of selective brain cooling, even during the hyperthermia which followed surgery or that associated with intense, short-duration exercise. The relationship between brain and arterial blood temperatures in free-ranging zebras was unlike that reported for horses in the laboratory. Our results do not support the view that mammals lacking a carotid rete can achieve selective brain cooling.

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Section: Discussioncontrasting

confidence: 68%

Section: Discussioncontrasting

confidence: 68%

Absence of Selective Brain Cooling in Free‐Ranging Zebras in Their Natural Habitat

Fuller

Maloney

Kamerman

et al. 2000

Experimental Physiology

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“…A second theory of SBC in humans, within the scalpsinus pathway, is ostensibly corroborated by the observation that tympanic temperature [used as a surrogate for brain temperature (280)] is reduced by a greater magnitude than esophageal or rectal during local head cooling while heat stressed (51,66,67,318). These findings, however, should be held with caution.…”

Section: Can the Brain Selectively Cool?mentioning

confidence: 93%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…However, to address this issue Nybo et al (209) investigated cerebral heat balance and measured the internal jugular venous blood temperature as index of the average brain temperature during exercise with and without hyperthermia. The controversial idea that humans, like some animal species, are capable of selectively cooling the brain during hyperthermia arose from the observation that the tympanic membrane temperature may be reduced below other core temperature sites (esophageal or rectal), if active cooling is applied to the head (29,33,34); (185). However, it is important to emphasize that, although the tympanic membrane is located close to the surface of the brain, it is neither a true nor reliable index of the global brain temperature (209,210,284).…”

Section: Cerebral Heat Balancementioning

confidence: 99%

Performance in the Heat—Physiological Factors of Importance for Hyperthermia‐Induced Fatigue

Nybo

Rasmussen

Sawka

2014

Comprehensive Physiology

262

299

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This article presents a historical overview and an up-to-date review of hyperthermia-induced fatigue during exercise in the heat. Exercise in the heat is associated with a thermoregulatory burden which mediates cardiovascular challenges and influence the cerebral function, increase the pulmonary ventilation, and alter muscle metabolism; which all potentially may contribute to fatigue and impair the ability to sustain power output during aerobic exercise. For maximal intensity exercise, the performance impairment is clearly influenced by cardiovascular limitations to simultaneously support thermoregulation and oxygen delivery to the active skeletal muscle. In contrast, during submaximal intensity exercise at a fixed intensity, muscle blood flow and oxygen consumption remain unchanged and the potential influence from cardiovascular stressing and/or high skin temperature is not related to decreased oxygen delivery to the skeletal muscles. Regardless, performance is markedly deteriorated and exercise-induced hyperthermia is associated with central fatigue as indicated by impaired ability to sustain maximal muscle activation during sustained contractions. The central fatigue appears to be influenced by neurotransmitter activity of the dopaminergic system, but inhibitory signals from thermoreceptors arising secondary to the elevated core, muscle and skin temperatures and augmented afferent feedback from the increased ventilation and the cardiovascular stressing (perhaps baroreceptor sensing of blood pressure stability) and metabolic alterations within the skeletal muscles are likely all factors of importance for afferent feedback to mediate hyperthermia-induced fatigue during submaximal intensity exercise. Taking all the potential factors into account, we propose an integrative model that may help understanding the interplay among factors, but also acknowledging that the influence from a given factor depends on the exercise hyperthermia situation.

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Selective brain cooling in hyperthermia: the mechanisms and medical implications

Cited by 41 publications

References 21 publications

Absence of Selective Brain Cooling in Free‐Ranging Zebras in Their Natural Habitat

Absence of Selective Brain Cooling in Free‐Ranging Zebras in Their Natural Habitat

Cerebral Vascular Control and Metabolism in Heat Stress

Performance in the Heat—Physiological Factors of Importance for Hyperthermia‐Induced Fatigue

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