The influence of systemic arterial pressure and intracranial pressure on the development of cerebral vasogenic edema

Abstract

The influence of intracranial pressure (ICP), systemic arterial pressure (SAP), and cerebral perfusion pressure (CPP) upon the development of vasogenic cerebral edema is largely unknown. To study their relationship, the authors have produced an osmotic disruption of the blood-brain barrier unilaterally in rabbits by injecting 1 cc/kg of 2M NaCl into the left internal carotid artery. The amount of vasogenic edema produced was assessed by quantitation of the extravasation of Evans blue dye into the area of maximum blood-brain barrier breakdown by means of optical densitometry following formamide extraction. The ICP was measured using a cisterna magna catheter into which mock cerebrospinal fluid could be infused at a predetermined pressure. The SAP was controlled by exsanguination from a femoral artery catheter. In 18 animals in which blood pressure was not controlled, no significant relationship between the ICP and the degree of Evans blue dye extravasation was noted. In these animals, however, a direct relationship between CPP (defined as mean arterial pressure minus mean ICP) and extravasation of Evans blue dye was found (correlation coefficient 0.630; p less than 0.001). When ICP was held constant at 0 to 5 mm Hg in another group of 16 animals and different levels of blood pressure were produced by exsanguination, a significant direct relationship between extravasation of Evans blue dye and the SAP was found (correlation coefficient 0.786; p less than 0.001). In a third group of 20 animals, the blood pressure was held constant at 90 to 100 mm Hg and the ICP was varied between 0 and 75 mm Hg. There was a highly significant result indicating increasing Evans blue dye extravasation with lower levels of ICP (p less than 0.001). Cerebral blood flow determinations by the hydrogen clearance method indicated loss of autoregulation in all animals in the areas of brain injured by intracarotid hypertonic saline. These results indicate that high SAP and low ICP (that is, a large CPP) promote Evans blue dye extravasation in this model of blood-brain barrier disruption. This finding has implications for the management of patients with vasogenic edema.

Blood–Brain Barrier Disruption, Vascular Impairment, and Ischemia/Reperfusion Damage in Diabetic Stroke

“…Immediately following ischemic injury, cytotoxic cerebral edema may ensue, driven by impaired cellular metabolism and dysfunction of sodium and potassium membrane ion pumps, which leads to increased water uptake and subsequent swelling of brain cells 20. Vasogenic edema formation is driven by hydrostatic pressure gradient, which is influenced by intracranial pressure, systemic blood pressure, capillary occlusion, and vasospasm 19. In vasogenic edema, following TJ and BBB rupture, transendothelial permeability increases, facilitating the entry of water and plasma proteins such as albumin and immunoglobulin G into the brain interstitial space 21.…”

“…In vasogenic edema, following TJ and BBB rupture, transendothelial permeability increases, facilitating the entry of water and plasma proteins such as albumin and immunoglobulin G into the brain interstitial space 21. The osmotic pressure gradient mediated by osmotically active molecules such as Na + and proteins also mediates water influx in vasogenic edema 19. Poststroke brain edema was found to be associated with greater neurological deficits both during admission and at discharge 22.…”

Effects of Induced Hypertension on Intracranial Pressure and Flow Velocities of the Middle Cerebral Arteries in Patients With Large Hemispheric Stroke

“…10,[33][34][35] On the other hand, a high CPP has been shown to enhance edema formation in a rabbit model with induced blood-brain barrier disruption. 36 Induced hypertension used during a prolonged time or initiated after a time delay following experimental stroke could be compared better with the clinical situation but has not yet been sufficiently studied in animal models. In rabbits with temporary MCA occlusion, induced hypertension restored the diminished regional CBF to nearly previous levels and caused a 97% reduction in infarct size; however, the hypertensioninduced reduction in infarct size diminished with time, and there was no protective effect when hypertension was maintained during occlusions of greater than 1 hour.…”

Blood Pressure in Acute Stroke: Causes and Consequences

“…In the more ordinary stroke patient, arguments for acute treatment are the edema around a hemorrhage or an infarction that may increase if blood pressure is high (60). In experimental animals, a cerebral infarction may be transformed into a hemorrhagic infarction if the blood pressure is high (61).…”