[Effects of the cortical subarachnoid hemorrhage on cerebral glucose metabolism]

Abstract

Neurological deficits following human subarachnoid hemorrhage (SAH) have been related to the cerebral arterial spasm and the increase in intracranial pressure (ICP) secondary to the development of hydrocephalus. Metabolic depression in experiment study was thought as resulting from brain stem dysfunction. On the other hand, some reports have shown no relationship between vasospasm and neurological abnormalities. The mechanism of cerebral metabolism depression after SAH remains unclear. The effect of blood in the cortical subarachnoid space on the cerebral metabolism has not been known well. To investigate this effect, a new cortical SAH model was developed using rat and local cerebral glucose utilization (LCGU) after production of SAH was measured. A cortical SAH model: a small burr hole was made on the left parietal bone and the arachnoid membrane was pierced with a tapered glass-needle 60 mu tip in diameter. Fresh autologous non-heparinized arterial blood 0.04 ml was injected into subarachnoid space within 60 seconds through that needle. The blood extended over the left cerebral cortical surface with thin subarachnoid hematoma on the parietal cortex, but did not extend on the right hemisphere and the basal cistern. The increase in ICP during production of SAH was minimal, mean value of 7.2 mmHg and ICP slowly returned to the basal level within 30 minutes. Rats were divided into 3 groups; rats 2 hours (SAH-2h, n = 7) and 48 hours (SAH-48h, n = 7) after production of SAH and rats 2hours after 0.04 ml saline injection for control (Control, n = 7). LCGU was studied according to the methods developed by Sokoloff.(ABSTRACT TRUNCATED AT 250 WORDS)