Reversal of experimental acute cerebral vasospasm by angiotensin converting enzyme inhibition.
Author(s) -
P. J. D. Andrews,
N Papadakis,
Haralambos Gavras
Publication year - 1982
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.13.4.480
Subject(s) - medicine , subarachnoid hemorrhage , vasospasm , angiotensin converting enzyme , angiotensin ii , cerebral vasospasm , saline , anesthesia , angiography , renin–angiotensin system , aneurysm , cardiology , blood pressure , surgery
We tested the hypothesis that cerebral arteriospasm developing after rupture of a subarachnoid aneurysm may be due to the vasoconstrictor effect of locally generated angiotensin II. Ten dogs had subarachnoid hemorrhage simulated by intracisternal introduction of 2 ml autologous blood, and were followed by cineangiography. Thirty minutes later, when acute arteriospasm was established, seven dogs received injection of the angiotensin converting enzyme inhibitor teprotide and 3 control dogs received normal saline. Repeat angiography at 30 and 90 minutes after injection, showed total or partial release of spasm in the experimental dogs and no change or further intensification of spasm in the control animals. We concluded that angiotensin converting enzyme inhibition may be a potentially useful approach for the reversal or prevention of cerebral arteriospasm after subarachnoid hemorrhage.
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