Arterial hypertension increases intracranial pressure in cat after opening of the blood-brain barrier.

Background: Increased permeability for small solutes in brain capillaries means that a change in hydrostatic capillary pressure may influence transcapillary fluid exchange according to the Starling fluid equilibrium, and a high arterial pressure may cause transcapillary fluid filtration and raised intracranial pressure. This could be of clinical relevance in states of disrupted blood-brain barrier such as meningitis and after a severe head injury, especially since these patients quite often are spontaneously hypertensive, and hypertensive therapy is sometimes used to increase cerebral perfusion pressure. This study on cat investigated the long-term relation between arterial pressure and intracranial pressure in a state of disrupted blood-brain barrier. Method: Endotoxin was given intrathecally to open the blood-brain barrier and depress cerebral autoregulation. Arterial pressure was increased by about 30 mm Hg during 5 hours by dopamine and angiotensin II infusion. The immediate fall in intracranial pressure after normalization of blood pressure reflects the blood volume component of an intracranial pressure increase. Results: Increased arterial pressure had no effect on intracranial pressure before endotoxin. Endotoxin infusion increased intracranial pressure from the normal value of 10 to 12 mm Hg. and at steady state by almost 10 mm Hg. Intracranial pressure increased further after the arterial pressure increase. At steady state (achieved within 5 hours), this increase was almost as great as the arterial pressure increase, and about 80% persisted when measured directly after normalization of the arterial pressure. Conclusion: Increased arterial pressure in a state of disrupted blood-brain barrier increases intracranial pressure, mainly because of brain edema. This stresses that arterial hypertension may be deleterious in conditions such as meningitis or after a brain trauma.