Cerebral metabolism, oxidation and inflammation in severe passive hyperthermia with and without respiratory alkalosis
Bain AR, Hoiland RL, Donnelly J, Nowak-Flück D, Sekhon M, Tymko MM, Greiner JJ, DeSouza CA, Ainslie PN
The Journal of physiology · 21 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- Controlled clinical trial (classified by our AI screen)
- Studied in
- People
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- National Institutes of Health
- Government
- NIH HHS
- Grants
- National Institutes of Health (HL077450); National Institutes of Health (HL107715)
Based on 2 listed funder(s).
Publication
- Published
- 2020-01-04 · J Physiol · vol. 598 · issue 5 · pp. 943–954
- Publisher
- Wiley
- Cited
- 25 citations · more than 83% of similar papers · 1.6× the field average
- References
- 45 works
- Access
- Paywalled
- Research areas
- Thermoregulation and physiological responses · Thermal Regulation in Medicine · Climate Change and Health Impacts
- Keywords
- Respiratory alkalosis, Inflammation, Hyperthermia, Respiratory system, Medicine, Alkalosis, Metabolism, Cardiology, Anesthesia, Internal medicine, Acidosis, Metabolic acidosis
- MeSH
- brain, humans, alkalosis, respiratory, inflammation, fever, cerebrovascular circulation, male, hyperthermia
9 authors
From CA, GB, US
- Anthony Richard Bain · correspondingUniversity of Windsor
- Ryan L. HoilandInterior Health; University of British Columbia; University of British Columbia, Okanagan Campus
- Joseph E. DonnellyUniversity of Cambridge; Addenbrooke's Hospital
- Daniela Nowak‐FlückInterior Health; University of British Columbia; University of British Columbia, Okanagan Campus
- Mypinder S. SekhonInterior Health; University of British Columbia; University of British Columbia, Okanagan Campus
- Michael M. TymkoInterior Health; University of British Columbia; University of British Columbia, Okanagan Campus
Abstract
Key points
It was unknown whether respiratory alkalosis impacts the global cerebral metabolic response as well as the cerebral pro-oxidation and inflammatory response in passive hyperthermia. This study demonstrated that the cerebral metabolic rate was increased by ∼20% with passive hyperthermia of up to +2°C oesophageal temperature, and this response was unaffected by respiratory alkalosis. Additionally, the increase in cerebral metabolism did not significantly impact the net cerebral release of oxidative and inflammatory markers. These data indicate that passive heating of up to +2°C core temperature in healthy young men is not enough to confer a major oxidative and inflammatory burden on the brain, but it does markedly increase the cerebral metabolic rate, independently of PaCO2 .
Abstract
There is limited information concerning the impact of arterial PCO2 /pH on heat-induced alteration in cerebral metabolism, as well as on the cerebral oxidative/inflammatory burden of hyperthermia. Accordingly, we sought to address two hypotheses: (1) passive hyperthermia will increase the cerebral metabolic rate of oxygen (CMRO2 ) consistent with a combined influence of Q10 and respiratory alkalosis; and (2) the net cerebral release of pro-oxidative and pro-inflammatory markers will be elevated in hyperthermia, particularly in poikilocapnic hyperthermia. Healthy young men (n = 6) underwent passive heating until an oesophageal temperature of 2°C above resting was reached. At 0.5°C increments in core temperature, CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-jugular venous oxygen content difference (cannulation). Net cerebral glucose/lactate exchange, and biomarkers of oxidative and inflammatory stress were also measured. At +2.0°C oesophageal temperature, arterial PCO2 was restored to normothermic values using end-tidal forcing. The primary findings were: (1) while CMRO2 was increased (P 2 , irrespective of arterial pH.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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