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.

Subarachnoid Hemorrhage in the Rat: Cerebral Blood Flow and Glucose Metabolism during the Late Phase of Cerebral Vasospasm

“…(1970), Bruce et al (1972), andEklOf andSiesjo (1972) that the cerebral metabolism does not change in an anaerobic direction until the CBF is reduced by �50%. Thus, in normal animals a CBF reduction of up to 50% will be adequately balanced by an increased oxygen extraction, while in SAH animals there seems to be a reduction in CMR02, probably secondary to a decrease in the extraction rate of oxygen, as suggested by Fein (1975). Fein fo und an immediate decrease in CMR02 in mon keys fo llowing an acute SAH despite an initially preserved blood flow.…”

“…Fein (1975) fo und that the changes oc curred irrespective of whether or not blood was in jected under isobaric or hyperbaric conditions. Sahlin et aI.…”

“…Further evidence for an anaerobic glycolysis is provided by studies showing an increased lactate/pyruvate ratio in the CSF in SAH patients (Kagstrom et aI., 1973;Fujishima et aI., 1975;Pasqualin et aI., 1985). An increased lactate/pyruvate ratio has been found in the acute phase after an experimental SAH in dogs (Shannon et aI., 1972;Sugi et aI., 1975) and in monkeys (Fein, 1975). Fein (1975) also described an increased ratio in brain tissue obtained from rats in the acute phase after a SAH.…”

“…An increased lactate/pyruvate ratio has been found in the acute phase after an experimental SAH in dogs (Shannon et aI., 1972;Sugi et aI., 1975) and in monkeys (Fein, 1975). Fein (1975) also described an increased ratio in brain tissue obtained from rats in the acute phase after a SAH. The anaerobic glycol ysis can hardly be explained on the basis of re duced CBF.…”

“…Solomon et al (1985) measured hemispheric CBF in the acute stage using a microsphere tech nique, and. Fein (1975) did regional metabolic studies at selected time points during the first 12 h after SAH.…”