Reversal of experimental acute cerebral vasospasm by angiotensin converting enzyme inhibition.
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.
D000208:Acute Disease; D000804:Angiotensin II / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D002932:Cineangiography; D004195:Disease Models, Animal; D004285:Dogs; D002546:Ischemic Attack, Transient / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D008297:Male; D009842:Oligopeptides / Q000627:therapeutic use*; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D013722:Teprotide / Q000494:pharmacology / Q000627:therapeutic use*
D000806:Angiotensin-Converting Enzyme Inhibitors; D009842:Oligopeptides; D000804:Angiotensin II; D013722:Teprotide