Brain energy metabolism in the acute stage of experimental subarachnoid haemorrhage: Local changes in cerebral glucose utilization

Abstract

An experimental model was used to investigate acute alterations of cerebral metabolic activity in rats subjected to subarachnoid haemorrhage (SAH). Haemorrhages were produced in anaesthetized animals by injecting 0.3 ml of autologous, arterial nonheparinized blood into the cisterna magna. Control rats received subarachnoid injections of mock-cerebrospinal fluid to study the effect of sudden raised intracranial pressure, or underwent sham operation. Three hours after SAH rats were given an intravenous injection of [14C]-2-deoxyglucose. Experiments were terminated by decapitation, and the brains were removed and frozen. Regional brain metabolic activity was studied by quantitative autoradiography. In comparison with sham-operated controls, cerebral metabolic activity was diffusely decreased after SAH. Statistically significant decreases in metabolic rate were observed in 23 of 27 brain regions studied. Subarachnoid injections of mock-cerebrospinal fluid also produced depression of cerebral metabolic activity, but quantitatively these changes were not as pronounced and diffuse as in SAH rats. The present study shows that a widespread depression of brain metabolism occurs in the acute stage after experimental SAH and is probably secondary to the subarachnoid presence of blood itself and/or blood products.

Early metabolic alterations in edematous perihematomal brain regions following experimental intracerebral hemorrhage

“…Indeed, comparable findings of normal-to-elevated high-energy phosphate and glucose concentrations and reduced glucose utilization, indicative of decreased metabolic rates, have been reported in injured hemispheres following cold lesions, 4,27 fluidpercussion trauma, 11 and subarachnoid hemorrhage that is possibly due to blood products. 7 In addition, glycogen accumulation that is found in the perihematomal white and gray matter in our model and after a variety of experimental injuries is analogous to that observed under conditions that reduce metabolism, such as hypothermia and anesthesia. 35 Increases in carbohydrate substrate concentration in tissue following ICH may be due to the perihematomal plasma protein accumulation that we previously described in this model.…”

Simvastatin Administration Ameliorates Neurobehavioral Consequences of Subarachnoid Hemorrhage in the Rat

“…SAH was induced in 12 rats (Groups III and IV) by administering 300 lL of autologous blood into the subarachnoid space via the cisterna magna. Details of the procedure have been published previously (d'Avella et al, 1990(d'Avella et al, , 1993(d'Avella et al, , 1996Germanò et al, 1992Germanò et al, , 1994Germanò et al, , 1998bGermanò et al, , 2000Germanò et al, , 2002Germanò et al, , 2007Imperatore et al, 2000). Briefly, the atlanto-occipital membrane was exposed through a midline occipital incision.…”

“…This neurological injury has been ascribed mainly to ischemic phenomena, occurring either during the initial bleeding episode or as a consequence of macro-and microvascular alterations, which are presumably able to set in motion a global brain dysfunction at different levels (d'Avella et al, 1990(d'Avella et al, , 1996Delgado et al, 1986;Doczi, 1985;Doczi et al, 1986;Germanò et al, 1992Germanò et al, , 2000Jackowski et al, 1990;Johshita et al, 1990;Sasaki et al, 1985Sasaki et al, , 1986Siesjo, 1992aSiesjo, , 1992bZuccarello and Anderson, 1989). Therefore, detailed knowledge about the pathobiology of SAH is critical to develop new treatment strategies; pathophysiological and experimental data together have significant implications both for the management of SAH patients and for investigating the rationale of new pharmacological approaches.…”

“…For the past 20 years our laboratory has developed an experimental in vivo rodent model of SAH that has provided extensive information about changes induced by intracisternal blood injection on hemodynamic, angiographic, biochemical, pathophysiologic, and acute and chronic behavioral parameters, which correlate those changes in humans after SAH (d'Avella et al, 1990, 1996Germanò et al, 1992Germanò et al, , 1994Germanò et al, , 2000. This model has also enabled us to evaluate the effects of systemic administration of different pharmacological agents on these parameters (d'Avella et al, 1993;Germanò et al, 1998bGermanò et al, , 2002Germanò et al, , 2007Imperatore et al, 2000).…”

Cerebral circulation and metabolism in the acute stage of subarachnoid hemorrhage

“…3,12,15,16,19,20,24 However, the mechanism of the reduction in CBF and cerebral metabolism is not yet clearly understood, particularly the primary process. Previous studies have indicated that CBF reduction is due to an elevation in ICP, metabolic reduction due to disturbance in brainstem-mediated O 2 uptake, or metabolic reduction due to the direct effects of subarachnoid blood.…”