Local Cerebral Glucose Utilization during Intracerebral pH Changes

Abstract

The effect of ventriculocisternal perfusion with mock CSF with alkaline or acidic pH on the local CMRglu (LCMRglu) in the caudatoputamen was studied in artificially ventilated and relaxed rats. In control rats both lateral cerebral ventricles were perfused with mock CSF at pH 7.4. In the experimental series one cerebral ventricle was infused with normal mock CSF while the other was infused with mock CSF in which the pH was decreased or increased by changing [HCO-3]. LCMRglu was depressed in acidotic brain tissue while it was strongly increased in alkalotic brain tissue. The importance of these alterations in brain glucose metabolism for the homeostatic regulation of brain pH is discussed.

Hyperventilation following head injury: Effect on ischemic burden and cerebral oxidative metabolism*

“…In particular, hyperventilation can induce seizures (45) and enhance neuronal excitability (44,46). Our SEP data are in keeping with previous studies that demonstrate increases in cortical SEP amplitudes in humans with hypocapnia (49) and changes in cerebral glucose consumption (50,51) with experimentally induced changes in cerebral pH. We demonstrate that cortical excitability measured by the ES 50 correlates with regional CMRO 2 .…”

The effects of CO2 levels and body temperature on brain interstitial pH alterations during the induction of hypoxic-ischemic encephalopathy in newborn pigs

“…We showed previously that normoxic hypercapnia (21% O 2 , 20% CO 2 ) alone reduces pH brain to 6.77 ± 0.05 [ 8 ] thus, if lactate production/accumulation levels were similar, a more profound drop in pH brain during asphyxia than during hypoxia would be expected, however, these minimum pH brain values were virtually identical in these groups suggesting reduced lactate contribution to the acidosis in asphyxia. This inverse relationship between pCO 2 and brain lactate levels induced for instance by hypo or hyperventilation has long been known [ 28 , 29 ] and were shown to be dependent on local changes of the cerebral metabolic rate of glucose [ 30 ]. In summary, under normothermic conditions, a complex interaction of a number of factors appear to determine the pH brain response to hypoxic/ischemic insult: a more severe hypoxia, higher blood sugar level and higher cerebral blood flow all strongly promote acidosis, while less severe hypoxia, lower blood glucose and brain ischemia tend to reduce pH brain drops.…”

Brain tissue acid-base changes during ischemia

“…[1,21] Nakai, et al, [14] simultaneously measured CBF, pH, and glucose metabolism using triple-tracer autoradiography during MCA occlusion in rats. They found that CBF, glucose metabolism, and pH were all lower in the ischemic region of hyperglycemic rats.…”