Background: Intraoperative microvascular vasospasm occurs in response to numerous stimuli, including direct vascular manipulation, metabolic homeostasis, and intrinsic propensity. Vasospasm can lead to decreased blood flow, stasis, or anastomotic clotting; persistent vasospasm may lead to partial or even complete loss of the microvascular reconstruction. Several factors have been implicated in inducing vasospasm including cold temperature, traction on the vessel wall, bleeding, increased sympathetic tone, and circulating vasoconstrictors. There are no published management algorithms for postoperativemicrovascular arterial vasospasmand the underlying etiology behind this phenomenon has not been clearly elucidated. However, the majority of microsurgeons have encountered this problem at some point in their practice. There are two surgical fields that aremore familiarwith the phenomenon of postoperative arterial vasospasm—cardiac surgery and neurosurgery. A total of 20 articles were included, representing data on 14 vasodilator agents. Drugs not amenable to local intraoperative administration or not approved for clinical use in the United States were excluded. Agents were classified into five pharmacologic categories based on their primary mechanisms: phosphodiesterase inhibitors (papaverine, pentoxifylline, and amrinone), local anesthetics (lidocaine), calcium channel blockers (nicardipine, verapamil, nifedipine, and magnesium sulfate), direct vasodilators (sodium nitroprusside, prostaglandin E1, nitroglycerin, and hydralazine), and alpha antagonists (phentolamine and chlorpromazine). A simplified summary of the mechanisms of action of topical vasodilators on vascular smooth muscle cells