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Cerebral metabolism, oxidation and inflammation in severe passive hyperthermia with and without respiratory alkalosis
Author(s) -
Bain Anthony R.,
Hoiland Ryan L.,
Donnelly Joseph,
NowakFlück Daniela,
Sekhon Mypinder,
Tymko Michael M.,
Greiner Jared J.,
DeSouza Christopher A.,
Ainslie Philip N.
Publication year - 2020
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp278889
Subject(s) - hyperthermia , cerebral blood flow , medicine , respiratory alkalosis , respiratory system , cerebral circulation , anesthesia , middle cerebral artery , metabolic acidosis , ischemia
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 P aC O 2.Abstract There is limited information concerning the impact of arterial P C O 2/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 (CMRO 2 ) 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, CMRO 2 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 P C O 2was restored to normothermic values using end‐tidal forcing. The primary findings were: (1) while CMRO 2 was increased ( P < 0.05) by ∼20% with hyperthermia of +1.5–2.0°C, this was not influenced by respiratory alkalosis, and (2) although biomarkers of pro‐oxidation and pro‐inflammation were systemically elevated in hyperthermia ( P < 0.05), there were no differences in the trans‐cerebral exchange kinetics. These novel 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, despite it markedly increasing CMRO 2 , irrespective of arterial pH.