Catecholamine response to intracranial hypertension.
Pulmonary congestion, hemorrhage, and edema, produced in the experimental animal by various methods of disturbing the central nervous system, 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 is found concerning the expected role of catecholamines. In this study, 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 per minute, were noted. 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. It is not unlikely that these events are related not only to increased ICP, but also to the effects of physical distortion of the brain stem with structural, functional, and vascular alterations within it.
D000818:Animals; D001794:Blood Pressure; D002395:Catecholamines / Q000097:blood*; D004285:Dogs; D004298:Dopamine / Q000097:blood; D004837:Epinephrine / Q000097:blood; D006339:Heart Rate; D007427:Intracranial Pressure; D009638:Norepinephrine / Q000097:blood
D002395:Catecholamines; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine