Cerebral oxygenation and hyperthermia

Abstract

Hyperthermia is associated with marked reductions in cerebral blood flow (CBF). Increased distribution of cardiac output to the periphery, increases in alveolar ventilation and resultant hypocapnia each contribute to the fall in CBF during passive hyperthermia; however, their relative contribution remains a point of contention, and probably depends on the experimental condition (e.g., posture and degree of hyperthermia). The hyperthermia-induced hyperventilatory response reduces arterial CO2 pressure (PaCO2) causing cerebral vasoconstriction and subsequent reductions in flow. During supine passive hyperthermia, the majority of recent data indicate that reductions in PaCO2 may be the primary, if not sole, culprit for reduced CBF. On the other hand, during more dynamic conditions (e.g., hemorrhage or orthostatic challenges), an inability to appropriately decrease peripheral vascular conductance presents a condition whereby adequate cerebral perfusion pressure may be compromised secondary to reductions in systemic blood pressure. Although studies have reported maintenance of pre-frontal cortex oxygenation (assessed by near-infrared spectroscopy) during exercise and severe heat stress, the influence of cutaneous blood flow is known to contaminate this measure. This review discusses the governing mechanisms associated with changes in CBF and oxygenation during moderate to severe (i.e., 1.0°C to 2.0°C increase in body core temperature) levels of hyperthermia. Future research directions are provided.

Cerebral Vascular Control and Metabolism in Heat Stress

“…On average, however, whole body and local hyperthermia increases CMRO 2 in animals by 5% to 10%/ • C (62,72,321,322), and in exercising humans an increased core temperature by ∼1.7 • C increases CMRO 2 by 7% to 8%; values in magnitude smaller than posited by a Q 10 of 2 to 3. Several factors may explain this discrepancy, including increases in nonoxidative metabolism (166), changes in arterial CO 2 (133), or inadequate CBF to maintain cerebral oxygen tension (365), although the latter is speculative (26). Conversely, these findings may simply reflect an erroneously inflated Q 10 for cerebral tissue during hyperthermia.…”

“…In turn, it is vague whether experimental heat stress is in fact sufficient to elicit reductions in cerebral oxygenation. Indeed, reductions in cerebral oxygenation as assessed by NIRS during heat stress (307), is likely confounded by the increased cutaneous blood flow (121) [see discussion in (26)]. Nonetheless, estimations of cerebral mitochondrial oxygen tension from measures of CBF [using the Kety-Shmidt technique (234)] and arterial-jugular venous oxygen differences, suggest that hyperthermic compared to normal exercise decreased mitochondrial oxygen tension by ∼5 mmHg (365).…”

Quantitative pharmacokinetic–pharmacodynamic modelling of baclofen‐mediated cardiovascular effects using BP and heart rate in rats

“…Stimulation of GABA B receptors located in the hypothalamus, intermediolateral column and rostral raphe pallidus also alters CBT (Addae et al , ; Jackson and Nutt, ; Tupone et al , ; Quéva et al , ). Additionally, CBT and BP share a common sympathetic nervous system activation pathway (Bain et al , ). Thus, baclofen can activate thermoregulatory mechanisms through multiple targets in the CNS as well as in the periphery.…”

Restoring heat stress‐associated reduction in middle cerebral artery velocity does not reduce fatigue in the heat

“…The most prominent mechanism to prevent severe deoxygenation in both thermoneutral and hyperthermic conditions appears to be an elevated O 2 extraction, which seems capable of compensating for the observed decline in cerebral perfusion (Nybo et al., ; Trangmar et al., ). It also seems that a reduction of about 50% in CBF would be required to impair cerebral O 2 in such a way that it affects exercise (Bain et al., ). This further strengthens the assumption that cerebral O 2 under hyperthermic conditions is not limiting incremental exercise performance.…”