Arterial hypertension increases intracranial pressure in cat after openingof the blood-brain barrier

Background: Increased permeability for small solutes in brain capillaries m eans that a change in hydrostatic capillary pressure may influence transcap illary fluid exchange according to the Starling fluid equilibrium. and a hi gh arterial pressure may cause transcapillary fluid filtration and raised i ntracranial pressure. This could be of clinical relevance in states of disr upted blood-brain barrier such as meningitis and after a severe head injury , especially since these patients quite often are spontaneously hypertensiv e, and hypertensive therapy is sometimes used to increase cerebral perfusio n pressure. This study on cat investigated the long-term relation between a rterial pressure and intracranial pressure in a state of disrupted blood-br ain barrier. Method. Endotoxin was given intrathecally to open the blood-brain barrier a nd depress cerebral autoregulation. Arterial pressure was increased by abou t 30 min Hg during 5 hours by dopamine and angiotensin II infusion. The imm ediate 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 increa se. At steady state (achieved within 5 hours), this increase was almost as great as the arterial pressure increase, and about 80% persisted when measu red 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. Th is stresses that arterial hypertension may be deleterious in conditions suc h as meningitis or after a brain trauma.