1 Faculty of Biology and Medicine, Institute of Sports Sciences, University of Lausanne , Lausanne, Switzerland .
High Alt Med Biol. 2014 Apr;15(1):70-7. doi: 10.1089/ham.2013.1065. Epub 2014 Feb 21.
We describe a case of experimentally induced pre-syncope in a healthy young man when exposed to increased inspired CO2 in a background of hypoxia. Acute severe hypoxia (FIO2=0.10) was tolerated, but adding CO2 to the inspirate caused pre-syncope symptoms accompanied by hypotension and large reductions in both mean and diastolic middle cerebral artery velocity, while systolic flow velocity was maintained. The mismatch of cerebral perfusion pressure and vascular tone caused unique retrograde cerebral blood flow at the end of systole and a reduction in cerebral tissue oxygenation. We speculate that this occurrence of pre-syncope was due to hypoxia-induced inhibition of brain regions responsible for compensatory sympathetic activity to relative hypercapnia.
我们描述了一例在健康年轻男性中，当暴露于缺氧背景下吸入二氧化碳增加时发生的实验性预晕厥。急性严重缺氧（FIO2=0.10）可耐受，但在吸入气中添加 CO2 会引起预晕厥症状，伴有低血压和大脑中动脉平均速度和舒张压的大幅下降，而收缩期血流速度保持不变。脑灌注压和血管张力的不匹配导致收缩期末出现独特的逆行脑血流，并降低脑氧合。我们推测，这种预晕厥的发生是由于缺氧抑制了负责对相对高碳酸血症进行代偿性交感神经活动的脑区。
