Faculty of Human Kinetics, University of Windsor, Windsor, Ontario, Canada.
Faculty of Health and Social Development, Center for Heart Lung and Vascular Health University of British Columbia, Kelowna, British Columbia, Canada.
J Physiol. 2020 Mar;598(5):943-954. doi: 10.1113/JP278889. Epub 2020 Feb 11.
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 .
There is limited information concerning the impact of arterial /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 ) 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 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 was restored to normothermic values using end-tidal forcing. The primary findings were: (1) while CMRO 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 , irrespective of arterial pH.
在被动性体温过高中，呼吸性碱中毒是否会影响全球大脑代谢反应以及大脑的氧化和炎症反应尚不清楚。本研究表明，体温升高至食管温度升高 2°C 时，大脑代谢率增加约 20%，而呼吸性碱中毒对此反应没有影响。此外，大脑代谢的增加并未显著影响氧化和炎症标志物的净脑释放。这些数据表明，健康年轻男性核心体温升高至 2°C 以内不足以对大脑造成主要的氧化和炎症负担，但确实会显著增加大脑代谢率，而与无关。
关于动脉 pH 值对热诱导的大脑代谢改变以及体温过高的大脑氧化/炎症负担的影响，相关信息有限。因此，我们试图验证两个假设：（1）被动性体温过高将增加与 Q10 和呼吸性碱中毒共同作用的大脑耗氧量（CMRO ）；（2）在体温过高时，特别是在低碳酸血症性体温过高时，大脑中促氧化和促炎症标志物的净释放将会升高。健康的年轻男性（n=6）接受被动性加热，直到食管温度升高至基础值以上 2°C。在核心温度升高 0.5°C 的过程中，通过超声测量的脑血流和桡动脉-颈静脉氧含量差（导管）的乘积计算 CMRO 。还测量了净脑葡萄糖/乳酸交换以及氧化和炎症应激的生物标志物。在食管温度升高至+2.0°C 时，使用呼气末强迫使动脉恢复到正常体温。主要发现为：（1）尽管体温升高至+1.5-2.0°C 时 CMRO 增加（P<0.05）约 20%，但呼吸性碱中毒对此没有影响；（2）尽管体温过高时系统升高了促氧化和促炎症的生物标志物（P<0.05），但大脑内的交换动力学没有差异。这些新数据表明，健康年轻男性核心体温升高至+2°C 以内不足以对大脑造成主要的氧化和炎症负担，尽管它明显增加了 CMRO ，但与动脉 pH 值无关。
