Effects of arterial carbon dioxide manipulation on cerebral oxidative metabolism during hemorrhagic hypotension in dogs

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[Background] : Development of brain acidosis is concerned during prolonged hemor- rhagic hypotension due to blood-brain barrier disruption, even though cerebral blood flow is maintained. There is possibility that PaC02 manipulation affects brain acidosis induced deterioration of cerebral oxidative metabolism by influencing the brain acid- base equilibrium. [Methods] : A dog model of hemorrhagic hypotension was used. Mean arterial pressure was kept at the lower limit of autoregulation to assure maintained cerebral blood flow. One of three different PaC02 manipulations, hypocapnia, normocapnia or hy-percapnia, was applied during hypotension and the effect of PaC02 manipulations on cerebral oxidative metabolism was estimated. [Results] : Cerebral blood flow and cerebral metabolic rate for oxygen remained unal-tered during hypotension. Brain acidosis was developed regardless of the PaC02 ma-nipulation used, being most acidotic with hypercapnia. Hypercapnia was accompanied by a significant decrease in phosphocreatinine and an increase in the L/P ratio com-pared to hypocapnia and normocapnia. [Conclusions] : PaC02 manipulation differentially affects cerebral oxidative metabolism during hemorrhagic hypotension with preserved cerebral blood flow, being worse with hypercapnia.

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