Cerebral energy metabolism after subarachnoid hemorrhage.

Abstract

The purpose of this study was to determine the primary effects of subarachnoid hemorrhage (SAH) on cerebral oxidative metabolism and energy balance. Rhesus monkeys were prepared so that cerebral metabolic consumption rates of oxygen, glucose and the lactate/pyruvate ratios of CSF were estimated after isobarically and hyperbarically induced SAH. A regional analysis was performed on brain sections after similarly induced SAH in the rat, for levels of tissue, glucose, lactate, pyruvate, ATP, ADP, AMP, PCr and the partition of hexokinase between soluble and mitochondrial bound forms. The presence of intracranial hypertension was associated with an immediate ischemia, and increased cerebral glucose extraction was initially noted. Specific tissue substrate concentrations in rat brain indicated that fresh intracisternal hemorrhage is associated with decreased glycosis at a time when high energy phosphate levels are normal. It is concluded that intracranial hypertension hastens the onset of ischemia after SAH. SAH alone produces a decrease in cerebral energy requirements which secondarily depresses the rates of consumption of energy yielding substrates. The depression in metabolic rates may be mediated through a brain stem mechanism.