Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia

Department of Radiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism (Impact Factor: 5.41). 04/2011; 31(7):1504-12. DOI: 10.1038/jcbfm.2011.34
Source: PubMed


The effect of hypercapnia on cerebral metabolic rate of oxygen consumption (CMRO(2)) has been a subject of intensive investigation and debate. Most applications of hypercapnia are based on the assumption that a mild increase in partial pressure of carbon dioxide has negligible effect on cerebral metabolism. In this study, we sought to further investigate the vascular and metabolic effects of hypercapnia by simultaneously measuring global venous oxygen saturation (S(v)O(2)) and total cerebral blood flow (tCBF), with a temporal resolution of 30 seconds using magnetic resonance susceptometry and phase-contrast techniques in 10 healthy awake adults. While significant increases in S(v)O(2) and tCBF were observed during hypercapnia (P<0.005), no change in CMRO(2) was noted (P>0.05). Additionally, fractional changes in tCBF and end-tidal carbon dioxide (R(2)=0.72, P<0.005), as well as baseline S(v)O(2) and tCBF (R(2)=0.72, P<0.005), were found to be correlated. The data also suggested a correlation between cerebral vascular reactivity (CVR) and baseline tCBF (R(2)=0.44, P=0.052). A CVR value of 6.1%±1.6%/mm Hg was determined using a linear-fit model. Additionally, an average undershoot of 6.7%±4% and 17.1%±7% was observed in S(v)O(2) and tCBF upon recovery from hypercapnia in six subjects.

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Available from: Felix W Wehrli, Jan 09, 2015
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    • "Some of this inconsistency in results between human and animal studies can be attributed to the different physiological conditions under which the experiments were performed. However, the data in Jain et al (2011), Chen and Pike (2010) and Xu et al (2011) were obtained in normal awake humans, and one can only speculate that differences should be attributed to differences in experimental techniques. Substantial progress has been made in developing in vivo methods to study brain metabolism and hemodynamics since the initial publication (Kety and Schmidt, 1948), and the paper by Jain et al contributes significantly to this development. "
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