The angiopathy of subarachnoid hemorrhage I. Role of vessel wall catecholamines.
Author(s) -
Junji Yoshioka,
Ben R. Clower,
Robert R. Smith
Publication year - 1984
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.15.2.288
Subject(s) - medicine , subarachnoid hemorrhage , reserpine , angiopathy , norepinephrine , cats , catecholamine , blood vessel , anesthesia , cardiology , dopamine , endocrinology , diabetes mellitus
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.
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