The angiopathy of subarachnoid hemorrhage I. Role of vessel wall catecholamines.
- 29 February 1984
- journal article
- research article
- Published by Wolters Kluwer Health in Stroke
- Vol. 15 (2) , 288-294
- https://doi.org/10.1161/01.str.15.2.288
Abstract
Subarachnoid hemorrhage (SAH) due to rupture of the right middle cerebral artery (RMCA) produced specific anatomical and biophysiological responses in the involved feline vessels. The RMCA showed morphological alterations that became progressively more severe with time and were widespread within the cerebral vascular tree. SAH also resulted in an acute depletion of vessel catecholamine levels which remained depressed over a 30 day period. When the cerebral vessels of cats were severely depleted of catecholamines (using reserpine) prior to induced SAH, morphological alterations were significantly reduced both in severity and in degree of spread within the cerebral vascular network. The results of this study suggest that the concentration of norepinephrine within the vessel at the time of hemorrhage plays a significant role in the production of the angiopathy that follows SAH.This publication has 32 references indexed in Scilit:
- The three phases of vasospasmSurgical Neurology, 1982
- The pathophysiology of cerebral vasospasm, and pharmacological approaches to its managementActa Neurochirurgica, 1982
- Norepinephrine in cerebrospinal fluid of patients with cerebral vasospasmJournal of Neurosurgery, 1982
- Sympathetic nervous system activity in patients with subarachnoid hemorrhage.Stroke, 1978
- Experimental cerebral vasospasmJournal of Neurosurgery, 1975
- Experimental catecholamine-induced chronic cerebral vasospasmJournal of Neurosurgery, 1974
- Adrenergic innervation of the cerebral blood vessels in the rabbitJournal of Neurosurgery, 1971
- Effects of Reserpine on Calcium Levels in Cardiac Tissue of MiceCardiovascular Research, 1969