Changes in regional cerebral metabolism during  systemic hyperthermia in humans

Nunneley, Sarah A.; Martin, Charles C.; Slauson, James W.; Hearon, Christopher M.; Nickerson, Lisa D.; Mason, Patrick A.

doi:10.1152/japplphysiol.00072.2001

Cited by 61 publications

(62 citation statements)

References 28 publications

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“…Systemic hyperthermia significantly increases cerebral metabolic rate in adult humans (23%) (13), and in newborn pigs (65%) (12). In parallel with the increase in cerebral metabolic rate, there is a sharp (by 97%) rise in CBF in response to systemic hyperthermia in pigs (12).…”

Section: Discussionmentioning

confidence: 99%

“…However, it is unknown whether the collateral circulation is sufficient to meet increased cerebral metabolic demands. It is well established that systemic hyperthermia (fever) significantly increases cerebral metabolic demand and is associated with a steep increase in CBF (12,13). Given that permanent loss of the CAϩJV can potentially limit the rise in CBF in response to metabolic demand, we hypothesized that systemic hyperthermia/fever may induce cerebral ischemia in a hemisphere that has undergone CAϩJV ligation.…”

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confidence: 99%

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Systemic Hyperthermia Induces Ischemic Brain Injury in Neonatal Mice With Ligated Carotid Artery and Jugular Vein

et al. 2007

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Postnatal d 7 (p7) or p12 mice had their right carotid artery (CA) and jugular vein (JV) ligated to mimic veno-arterial (VA) access for extracorporeal membrane oxygenation (ECMO). At p9 -11 (early) or p19 -21 (late) mice were exposed to hyperthermia or normothermia followed by assessment of neuropathological injury score. In separate cohorts of mice, cerebral and peripheral blood flow (CBF, PBF) and cerebral ATP content was measured. Hyperthermia resulted in ischemic brain injury in 57% and 77% of mice subjected to early or late hyperthermia, respectively. Isolated CAϩJV ligation induced minimal injury (score 0.47 Ϯ 0.34) in 2/8 mice from the late normothermia group. No cerebral injury was detected in mice subjected to early normothermia. In 3/19 shams (2/10 early, 1/9 late) hyperthermia induced a subtle (score, 0.6 Ϯ 0.27) injury in the ipsilateral to the site of surgery cortex. CBF and PBF increased in response to hyperthermia in all mice. The rise in CBF was significantly attenuated in the "ligated" versus intact hemisphere, which was associated with a profound depletion of ATP content. Systemic hyperthermia induces ischemic brain injury in mice with ligated CAϩJV. We speculate that hyperthermia/fever can be a potential risk factor for brain injury in infants treated with VA ECMO.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Systemic Hyperthermia Induces Ischemic Brain Injury in Neonatal Mice With Ligated Carotid Artery and Jugular Vein

et al. 2007

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“…These authors reported glucose utilisation to be minimally altered or slightly higher in the thalamus and neocortex. Changes in regional cerebral metabolism have also been studied with FDG-PET in humans during steadystate hyperthermia [52]. This study reported a significant increase in FDG in the hypothalamus, thalamus, corpus callosum, cingulated gyrus and cerebellum, as well a significant decrease in the caudate, putamen, insula and posterior cingulum.…”

Section: Short-term Effects On Brain Glucose Metabolismmentioning

confidence: 94%

Effects of MDMA on blood glucose levels and brain glucose metabolism

Soto-Montenegro

Vaquero

Arango

et al. 2007

Eur J Nucl Med Mol Imaging

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Purpose This study was designed to assess changes in glucose metabolism in rats administered single or repeated doses of MDMA. Methods Two different experiments were performed: (1) A single-dose study with four groups receiving 20 mg/kg, 40 mg/kg, saline or heat, and (2) a repeated-dose study with two groups receiving three doses, at intervals of 2 h, of 5 mg/kg or saline. Rats were imaged using a dedicated small-animal PET scanner 1 h after single-dose administration or 7 days after repeated doses. Glucose metabolism was measured in 12 cerebral regions of interest. Rectal temperature and blood glucose were monitored. Results Peak body temperature was reached 1 h after MDMA administration. Blood glucose levels decreased significantly after MDMA administration. In the single-dose experiment, brain glucose metabolism showed hyperactivation in cerebellum and hypo-activation in the hippocampus, amygdala and auditory cortex. In the repeated-dose experiment, brain glucose metabolism did not show any significant change at day 7.Conclusion These results are the first to indicate that MDMA has the potential to produce significant hypoglycaemia. In addition, they show that MDMA alters glucose metabolism in components of the motor, limbic and somatosensory systems acutely but not on a long-term basis.

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“…It is generally accepted that heat stress, both passive and exertional, increases global CMRO 2 (325,326,365). Animal studies suggest that local cerebral and whole-body hyperthermia of up to 43 • C core temperature increase global cerebral glucose utilization (289, 296) and associated CMRO 2 by ∼5% to 10% per degree Celsius rise in core temperature (62,72,321,322).…”

Section: Metabolic Regulation Of Cerebral Blood Flow Cerebral Metabolismmentioning

confidence: 99%

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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Changes in regional cerebral metabolism during systemic hyperthermia in humans

Cited by 61 publications

References 28 publications

Systemic Hyperthermia Induces Ischemic Brain Injury in Neonatal Mice With Ligated Carotid Artery and Jugular Vein

Systemic Hyperthermia Induces Ischemic Brain Injury in Neonatal Mice With Ligated Carotid Artery and Jugular Vein

Effects of MDMA on blood glucose levels and brain glucose metabolism

Cerebral Vascular Control and Metabolism in Heat Stress

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