Reversal of experimental delayed cerebral vasospasm by angiotensin-converting enzyme inhibition.
Delayed cerebral vasospasm is an important determinant of the clinical outcome after subarachnoid hemorrhage, but its prevention and treatment has met with limited success. Since cerebral arteries were found to be sensitive to the vasoconstrictor effect of angiotensin II, the possibility of angiotensin's contribution to this vasospasm was investigated. Delayed cerebral arterial spasm was documented angiographically 72 hours after introduction of blood in the subarachnoid space of dogs. Following injection of the angiotensin-converting enzyme inhibitor, teprotide, repeat cineangiograms at 30, 60, and 90 minutes demonstrated partial or total release of spasm of the basilar artery and its branches. It is concluded that angiotensin II participates in the delayed cerebral vasospasm after hemorrhage, and that angiotensin inhibition may release the spasm and prevent cerebral ischemia.
D000792:Angiography; D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D001158:Arteries / Q000503:physiopathology; D001488:Basilar Artery / Q000503:physiopathology; D004285:Dogs; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology; D013722:Teprotide / Q000494:pharmacology; D013997:Time Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D013722:Teprotide