Cerebral Vascular Control and Metabolism in Heat Stress

被引:70
作者
Bain, Anthony R. [1 ]
Nybo, Lars [2 ]
Ainslie, Philip N. [1 ]
机构
[1] Univ British Columbia, Sch Hlth & Exercise Sci, Ctr Heart Lung & Vasc Hlth, Kelowna, BC, Canada
[2] Univ Copenhagen, Dept Nutr Exercise & Sport Sci, Copenhagen, Denmark
关键词
BLOOD-BRAIN-BARRIER; SYMPATHETIC-NERVE ACTIVITY; WHOLE-BODY HYPERTHERMIA; CEREBROVASCULAR CO2 REACTIVITY; CEREBROSPINAL FLUID BARRIER; ARTERIAL BAROREFLEX CONTROL; CUTANEOUS VASOCONSTRICTOR RESPONSES; SEVERE PASSIVE HYPERTHERMIA; AUTONOMIC NEURAL-CONTROL; STELLATE GANGLION BLOCK;
D O I
10.1002/cphy.c140066
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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 degrees C core temperature), the associated reduction in CBF (similar to 30%) and increase in cerebral metabolic demand (similar to 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. (C) 2015 American Physiological Society.
引用
收藏
页码:1345 / 1380
页数:36
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