In the mid 1960s, Mullan and Dawley,1 in the course of experimental work, noted that electrically induced thrombi in the femoral artery of dogs, which were normally of short duration, could be made to last longer when the antifibrinolytic agent ∈-aminocaproic acid was administered. This observation induced them to use the same agent in an attempt to prevent recurrent hemorrhage in patients who had recently suffered subarachnoid hemorrhage from ruptured aneurysms. In 1965, Norlén and Thulin2 had found the same agent to be of value during the surgery on two cases of arteriovenous malformations. This also had led them to employ antifibrinolytic agents in the management of ruptured saccular aneurysms, virtually simultaneously with Mullan and Dawley. The reasoning in both investigations was similar. If the dissolution of the hemostatic clot at the site of rupture could be delayed, the definitive operative procedure for the repair of the
Weir B. Antifibrinolytics in Subarachnoid Hemorrhage: Do They Have a Role? No. Arch Neurol. 1987;44(1):116–118. doi:10.1001/archneur.1987.00520130090025
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