Abstract
We examined the effect of IH (10% O2) conditioning on cerebral perfusion and oxygenation of 8 healthy volunteers (25.0±1.1 yr). The study was approved by IRB at UNTHSC. IH started with 5 bouts of 5‐min exposure alternating with 4‐min inhalation of room air and progressively increased to 10 bouts of 6‐min exposure on Day 7 through Day 14. Middle cerebral arterial blood flow velocity (VMCA) and regional cerebral O2 saturation (ScO2) were continuously measured during rebreathing (~6 min) induced increases in PETCO2. Continuous cerebral vascular conductance (CVC, the ratio of VMCA to mean arterial pressure) and ScO2 were averaged every 30 sec and the rate of % changes (Ä) during hypercapnia was compared. The rebreathing progressively raised PETCO2 from 41.4±1.1 to 56.6±1.5 mmHg pre and from 40.2±0.9 to 54.6±1.6 mmHg post, which were not statistically different pre and post IH conditioning. In response to unit hypercapnia, the rate of increases in group CVC was greater (P < 0.01) pre (2.87±0.16 %/mmHg) than post (2.12±0.12 %/mmHg); whereas the rate of increases in group ScO2 was smaller (P < 0.01) pre (1.08±0.04 %/mmHg) than post (1.22±0.04 %/mmHg). The slope of ÄScO2/ÄCVC was augmented (P < 0.01) following IH conditioning, i.e., pre vs post: 0.37±0.02 vs 0.56±0.03. Two‐week IH conditioning enhanced cerebral tissue oxygenation during hypercapnia even though cerebral arterial vasodilation to CO2 stimulus was diminished.
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