In order to study effects of increased cerebrospinal fluid pressure upon brain tissue concentrations of bicarbonate, lactate, pyruvate, ATP, ADP, AMP and phosphocreatine, the metabolites were measured in cortical tissue of 37 dogs frozen in situ during and after a 15 min decrease of the cerebral perfusion pressure to 30–35 mm Hg, induced by connecting the cisterna magna to a reservoir with artificial CSF. The intracranial hypertension was found to give a variable but marked increase in tissue lactate and pyruvate, and in the lactate/pyruvate ratio, as well as a corresponding decrease in the bicarbonate concentration. Marked decreases in the ATP and phosphocreatine concentrations were also seen. Resting values for these metabolites were not approached until 30–90 min after restitution of normal perfusion pressure. Since the changes in ATP and phosphocreatine corresponded in time to the changes in the lactate, pyruvate and bicarbonate concentrations it is concluded that the decrease in the cerebral perfusion pressure gave rise to a longlasting disturbance of the oxidative metabolism, possible due to reversible structural tissue damage. Cerebral blood flow measured in 10 of the dogs showed varying decreases of cerebral blood flow during the intracranial hypertension period. Usually, hyperemia of 30–90 min duration followed when the CSF pressure was released. The hyperemia and the metabolic changes were of approximately the same duration.
No takes yet. Share an insight, caveat, or question.
N. N. Zwetnow (1970) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: