THE PATHOGENESIS of cerebral vasospasm remains unclear, in spite of recent, extensive experimental investigations.1-3 No substance has been identified which can be labelled, with assurance, the vasoactive material responsible for clinical vasospasm, and more than one agent or stimulus may be involved, since the events leading to clinically demonstrable spasm are heterogenous.4 Most studies of experimental spasm have directed attention toward the large arteries of the brain,1-3 probably because the limitations of diagnostic radiology make it difficult to establish the existence of arteriolar spasm in the clinical situation.4 Nevertheless, profound constriction of arterioles over the convexity of the brain can be produced,5-10 and it seems advisable to supplement our studies of spasm with continued investigations of these small vessels.
In order to facilitate these investigations, it seems reasonable to employ a stimulus which elicits the largest constrictions of which the vessels are capable. Paradoxically, normal
Rosenblum WI. Cerebral Arteriolar Spasm Inhibited by β-Adrenergic Blocking Agents. Arch Neurol. 1969;21(3):296–302. doi:10.1001/archneur.1969.00480150086011
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