Experimental acute hepatic encephalopathy: relationship of pathological cerebral vasodilation to increased intracranial pressure.

In clinical reports of encephalopathy and pediatric trauma, acute brain swelling has been postulated to be secondary to vasodilation of the cerebrovascular bed. Eight adult cats were studied to determine whether such pathological vasodilation was present in an experimental model of hepatic encephalopathy. All animals were anesthetized, ventilated, and monitored for intracranial pressure (ICP), arterial pressure, heart rate, arterial blood gases, temperature, and blood ammonia content. The regional cerebral blood flow (rCBF) was measured at three cortical sites by the hydrogen clearance technique. The intravenous infusion of ammonium acetate was used to produce blood ammonia levels comparable to those observed in severe Reye's syndrome. All experimental animals showed a significant increase in ICP as well as rCBF to a mean of 79.5 +/- 7.3 ml/100 g/minute. This represents a mean increase in %rCBF to 252% of control. The mean calculated cerebrovascular resistance (CVR) was noted to fall to 55 +/- 4.7% of control CVR values (p less than 0.001). This relative vasodilation was diffuse with no significant difference between hemispheres or lobes studied. Such a vasodilation, as shown by a marked fall in the resistance of the cerebrovascular bed, is a pathological response in light of the rising ICP. This suggests that pathological cerebral vasodilation may be an important cause of increased ICP in the brain suffering an acute generalized insult.