Cerebral blood flow response to acute hypoxic hypoxia.
Bottom Line: However, this response, particularly at the tissue level, is not well characterised.The rate constant, temporal delay and magnitude of the CBF response were characterised using an exponential model for whole-brain and regional grey matter.The delay and rate constant for changes in R2 * were 24 s (95% CI: 21 s, 26 s) and 0.0392 s(-1) (95% CI: 0.0333 s(-1), 0.045 s(-1)), respectively, for the hypoxic response, and 12 s (95% CI: 10 s, 13 s) and 0.0921 s(-1) (95% CI: 0.0744 s(-1), 0.1098 s(-1)/) during the return to normoxia, confirming rapid changes in blood oxygenation with the end-tidal forcing system.
Affiliation: CUBRIC, School of Psychology, Cardiff University, Cardiff, UK.Show MeSH
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Mentions: During the hypoxic challenge, according to pulse oximetry, subjects desaturated to an average Spo2 of 83%, with the subject-averaged data reaching this level after 810 s. Group-averaged total oxygen delivery at baseline was 15.1 mL/100 g/min and, in hypoxia, was 14.7 mL/100 g/min, assuming that the dissolved oxygen is negligible 13 and that the concentration of haemoglobin (assumed to be 15 g/dL) does not change during the challenge. A summary of the physiological data is shown in Table 1. Sample CBF maps are shown in Fig. 2, and group-averaged end-tidal O2 and CO2 are shown in Fig. 3. Although the inclusion of the dynamic changes in T1, R2* and tissue arrival times is expected to reduce bias in the estimates for CBF in hypoxia, these refinements have the capacity to add noise in the calculated CBF time series, for example, when noise is already present in the R2* estimate as a result of head motion. As a result of nonconvergence of the numerical estimates of CBF, time-course data from three regions from one subject and one from another were excluded from the regional CBF estimates.
Affiliation: CUBRIC, School of Psychology, Cardiff University, Cardiff, UK.