Cerebral metabolic rate of oxygen

HI based on their findings of incomplete recovery of NTP. However, as the cerebral metabolic rate of oxygen did not correlate with any metabolic changes, they concluded impaired mitochondrial function could not be the only factor. 

Central nervous system. Thiopental has no analgesic activity and may be antanalgesic. It is a potent anticonvulsant. Cerebral metabolic rate of oxygen consumption (CMRO ) is reduced, which leads to cerebral vasoconstriction with a concomitant reduction in cerebral blood flow and intracranial pressure. 

Sevoflurane has a dose-dependent effect on cerebral blood flow and intracranial pressure cerebral autoregulation is preserved (this is not the case with isoflurane). During hypocarbia, in the absence of nitrous oxide, 1 MAC does not increase intracranial pressure (ICP). It reduces the cerebral metabolic rate for oxygen (CMR02) by approximately 50% at concentrations approaching 2 MAC. This is similar to the reduction observed during isoflurane anaesthesia. 

Desflurane reduces cerebral metabolic rate for oxygen (CMR02) to a similar extent as isoflurane. Cerebral vascular resistance is reduced and is accompanied by an increase in cerebral blood flow (0.5-2.0 MAC). It suppresses EEC activity and there is no evidence of epileptiform activity. Somatosensory evoked potentials are preserved at clinical concentrations. 

Positron emission tomographic (PET) studies may reveal a reduced cerebral metabolic rate for oxygen utilization, while single-photon emission computed tomographic (SPECT) studies can ascertain strokes in individuals with MELAS by using a tracer, /V-isopropyl-p- 123-1 -iodoamphetamine. The tracer accumulates in the parietooccipital region, and it can delineate the extent of the lesion. SPECT studies are used to monitor the evolution of the disease. 

Intracarotid infusion of PAF results in decreased cerebral blood flow with a concomitant increase in the global cerebral metabolic rate for oxygen (Kochanek et al, 1988, 1990). PAF administration causes a dose-dependent decrease in... 

Cerebral metabolic rate declines from developmental levels and plateaus after maturation. Reliable quantitative data on the changes in cerebral circulation and metabolism in humans from the middle of the first decade of life to old age have been reported [2,39,44]. By 6 years of age, cerebral blood flow and oxygen consumption already have attained high rates, and they decline thereafter to the rates of normal young adulthood [45]. Oxygen is utilized in the brain almost entirely for the oxidation of carbohydrates [46]. The equation for the complete oxidation of glucose is ... 

Severe, acute reduetion in oxygenation, for example by complete arrest of uterine flow or complete umbiheal cord occlusion, is not associated with a decrease in eerebrovascular resistance, as is seen in more mild insults. This suggests that the ability of the fetus to adapt to hypoxia has been overwhelmed. The rate at which the fetal arterial O2 content falls may be a determinant of the response elicited whether it be a rapid onset of ECoG isoelectricity (32,120), reduced regional cerebral blood flows (17), a failure of cardiovascular adaptive responses (139), an increase in eerebral lactate production (140), or a 50% reduction in cerebral metabolic rate... 

Measurements of regional cerebral blood flow by PET and of cerebral perfusion by SPECT often detect functional abnormalities before CT or MRI identifies morphological abnormalities 945 The PET method is a valuable tool for the estimation of regional glucose and oxygen metabolic rates and cerebral blood flow 946 PET and SPECT combined with principles of receptor binding permit imaging of receptors in the intact brain 946... 

Torbati D, Greenberg JH, Lambertsen CJ. Regional cerebral glucose metabolic rate during thirty minutes hypoxia of 7% oxygen in adult conscious rats. Neurosci Lett 1986 65 253-258. 

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