Catecholamine response to intracranial hypertension

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Abstract
Pulmonary congestion, hemorrhage and edema produced in the experimental animal by various methods of disturbing the CNS, have led to the concept that such neurogenically-initiated changes are mediated through the autonomic nervous system. Blocking the sympathetic nervous mechanisms prevents these changes. Little was found concerning the expected role of catecholamines. Using a standard model of increasing intracranial pressure (ICP), intense cardiovascular changes, with blood pressure rising above 320 mm Hg and heart rate of 180 beats/min were studied in the dog. Within seconds, plasma catecholamine levels rose as much as 1200 times the highest normal values for epinephrine, 145 times for norepinephrine and 35 times for dopamine. These changes occurred only when raised ICP was sustained and spatial compensation of the brain was exceeded. These events are possibly related to both increased ICP and to the effects of physical distortion of the brain stem with structural, functional and vascular alterations within it.