|dc.description.abstract||The influence of intracranial pressure, systemic arterial pressure and cerebral perfusion pressure upon the development of vasogenic cerebral oedema is largely unknown. To study their relationship, an osmotic disruption of the blood-brain barrier was produced unilaterally in female rabbits by injecting 1 cc/Kg of 2 M Na Cl into the left internal carotid artery. The amount of vasogenic oedema produced was assessed by quantitation of the amount of Evans Blue extravasation into the area of maximum blood-brain barrier breakdown by optical densitometry following Formamide extraction of the Evans Blue from the oedematous cortex. Intracranial pressure was measured using a cisterna magna catheter into which mock CSF could be infused to a predetermined pressure. Systemic arterial pressure was controlled by exsanguination from a femoral artery catheter in those animals selected for blood pressure control.
In the initial 18 animals in which blood pressure was not controlled, no significant relationship between the intracranial pressure and the degree of Evans Blue extravasation was noted. In these animals, however, a significant direct relationship between cerebral perfusion pressure (defined as mean arterial pressure minus mean intracranial pressure) and Evans Blue extravasation was found (correlation coefficient = .630, p ˂ .001). When intracranial pressure was maintained constant at 0-5 mmHg in 16 animals and different levels of blood pressure were produced by exsanguination, a significant direct relationship between Evans Blue extravasation and the systemic arterial pressure was found (correlation coefficient= .786,p <.001). In 20 animals the blood pressure was maintained constant at 90-100 mmHg and the intracranial pressure was varied between 0, 25, 50 and 75 mmHg with five animals at each pressure. There was a significant correlation indicating increasing Evans Blue extravasation at low levels of intracranial pressure (p (.001). This relationship may be exponential.
Cerebral blood flow determinations by the H2 clearance method indicated loss of autoregulation in the areas of brain injured by the intracarotid hypertonic saline. In addition, a progressive fall in the cerebral blood flow with time was noted in the same areas. Electron microscopic studies of cortical samples demonstrated abnormal amounts of extracellular fluid in the neuropil surrounding capillaries, and swelling of astrocytic foot processes. Inter-endothelial tight junctions were not disrupted.
These results indicate a high systemic arterial pressure and low intracranial pressure (i.e. a large cerebral perfusion pressure) promote Evans Blue extravasation in this model of blood-brain barrier disruption. This finding has implications for the management of patients with vasogenic oedema. Vigorous control of intracranial hypertension and/or failure to treat systemic arterial hypertension may have detrimental consequences by promoting increased cerebral oedema.||en_NZ