====== Respiratory alkalosis ======

It is unknown whether respiratory [[alkalosis]] impacts the global cerebral metabolic response as well as the cerebral pro-oxidation and [[inflammatory response]] in passive [[hyperthermia]]. 

A 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 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 from the [[PaCO2]]. 

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, Bain et al. sought to address two hypotheses, that; 1) passive hyperthermia will increase the cerebral metabolic rate of oxygen (CMRO2 ) consistent with 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. At 0.5°C increments in core temperature, the 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 the CMRO2 was increased (P < 0.05) by ∼20% with hyperthermia of +1.5°C to +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 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 [[CMRO2]], which is irrespective of arterial [[pH]]
((Bain AR, Hoiland RL, Donnelly J, Nowak-Flück D, Sekhon M, Tymko MM, Greiner
JJ, DeSouza CA, Ainslie PN. Cerebral metabolism, oxidation, and inflammation in
severe passive hyperthermia with and without respiratory alkalosis. J Physiol.
2020 Jan 3. doi: 10.1113/JP278889. [Epub ahead of print] PubMed PMID: 31900940.
)).