Regional cerebral metabolic rate (positron emission tomography) during inhalation of nitrous oxide 50% in humans
ABSTRACT Recent studies in man have shown that cerebral blood flow increases during inhalation of nitrous oxide (N2O), a finding which is believed to be a result of an increased cerebral metabolic rate (CMR). However, this has not previously been evaluated in man.
Regional CMR(glu) (rCMR(glu)) was measured three dimensionally with positron emission tomography (PET) after injection of 2-(18F)fluoro-2-deoxy-D-glucose in 10 spontaneously breathing men (mean age 31 yr) inhaling either N2O 50% in O2 30% or O2 30% in N2.
Global CMR(glu) in young men was 27 (3) micromol 100 g(-1) min(-1) [mean (SD)]. Inhalation of N2O 50% did not change global CMR(glu) [30 (5) micromol 100 g(-1) min(-1)] significantly, but it changed the distribution of the metabolism in the brain (P<0.0001 analysis of variance). Compared with inhalation of O2 30% in N2, N2O 50% inhalation increased the metabolism in the basal ganglia [14 (17)%, P<0.05] and thalamus [22 (23) %, P<0.05]. There was a prolonged metabolic effect of N2O inhalation seen on a succeeding PET scan with oxygen-enriched air (P<0.0001) performed 1 h after the N2O administration.
Inhalation of N2O 50% did not change global CMR(glu), but the metabolism increased in central brain structures, an effect that was still present 1 h after discontinuation of N2O.
- Advances in Anesthesia 01/2012; 30(1):29–46. DOI:10.1016/j.aan.2012.07.001
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ABSTRACT: The effects of xenon on regional cerebral blood flow (rCBF) are controversial. Moreover, the precise sites of action at which xenon exerts its effects in the human brain remain to be established. rCBF was sequentially assessed by H(2)(15)O positron emission tomography in six volunteers. rCBF was determined at baseline and during general anaesthesia induced with propofol and maintained with one minimum alveolar concentration xenon. rCBF measurements were started after the calculated plasma concentration of propofol had decreased to subanaesthetic levels (<1.0 microg ml(-1)). Changes in rCBF were calculated for 13 cerebral volumes of interest by measurement of a semi-quantitative perfusion index (PI). In addition, voxel-wise changes in rCBF were analysed using statistical parametric mapping. Xenon had only minor effects on PI in grey matter volumes of interest. In contrast, PI was increased in white matter [from 1.01 (0.11) to 1.24 (0.15) kcnt ml(-1) MBq(-1), P=0.05, mean (SD)]. Voxel-based analysis showed an increase of rCBF in white matter and a relative decrease of rCBF during xenon anaesthesia in distinct grey matter regions, particularly the orbito- and mesiofrontal cortex, cingulate gyrus, thalamus, hippocampus and bilateral cerebellum (P<0.05 corrected). When correlating PI with cerebral metabolic rate of glucose (previously obtained in another group of six volunteers using (18)F-fluorodeoxyglucose as tracer), the flow-metabolism coupling was preserved during xenon anaesthesia. Xenon exerted distinct regional effects on CBF: relative decreases in several cortical, subcortical, and cerebellar areas were accompanied by an increase in white matter. Flow-metabolism coupling was not impaired during xenon anaesthesia.BJA British Journal of Anaesthesia 06/2008; 100(5):667-75. DOI:10.1093/bja/aen036 · 4.85 Impact Factor
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ABSTRACT: This review will highlight the recent functional magnetic resonance imaging, positron emission tomogram scan and connectivity studies in anesthesia and analgesia. In regional cerebral blood flow (rCBF) studies with isoflurane and sevoflurane, there is a consistent pattern of rise in rCBF in the anterior cingulate cortex and insula while the thalamus, lingual cortex and cerebellum show a decrease in rCBF, in a dose range of 0.2-1 minimum alveolar concentration. Even 0.25 minimum alveolar concentration causes a predominant decrease of rCBF in the cortical regions and increase of rCBF in the subcortical regions. This minimum alveolar concentration level primarily affects the association cortices. Thalamus and thalamo-cortical pathways seem to be linked to the hypnotic effects of anesthesia and deep sedation. Connectivity studies also confirm this. The electroencephalogram equivalent of this appears to be a transition from 'alpha' wave activity to 'delta' wave activity. Anterior cingulate cortex, S1 and S2 are the regions consistently activated in acute pain. Remifentanil infusion in acute pain decreases the activation in pain perception regions while activating the pain modulation regions. In chronic pain states, prefrontal cortex and insula are activated whereas there is a decrease in activity in the thalamus. Slowly, a pattern of neuronal activity reflecting hypnosis, analgesia, amnesia and reflex suppression seems to be emerging giving us a better insight into the central nervous system effects of anesthesia.Current opinion in anaesthesiology 11/2008; 21(5):530-6. DOI:10.1097/ACO.0b013e32830edbf3 · 1.98 Impact Factor