Analyses of improvements in nerve conduction velocity (NCV) and blood flow after administering cilostazol in a dog model of experimental acute and chronic cauda equina compression. To determine whether cilostazol improves NCV and blood flow, and cilostazol inhibits blood clots in capillaries of nerve roots after cauda equina compression. Reduction in blood flow is an important factor in neurogenic intermittent claudication for lumbar spinal stenosis. Prostaglandin E1 (PGE1) and calcitonin have been reported to improve blood flow and neurogenic intermittent claudication in clinical and experimental studies. Cilostazol affects vasodilator and antiplatelet activity, and protects endothelial cells in blood vessels. Experimental groups in the acute compression study (n = 40) were divided into 4 treatment groups. Low-dose (3 microg/kg/min), medium-dose (10 microg/kg/min), or high-dose (30 microg/kg/min) cilostazol or a control vehicle were administered intravenously after cauda equina compression. NCV and blood flow were measured during the observation period (n = 20 measurements for each). Another 12 animals were used to evaluate chronic compression. Cilostazol was administered for 6 days orally 1 day after compression treatment group (n = 6); the nontreatment group (n = 6) did not receive any drug. NCV was measured immediately after and 7 days after compression. Blood flow was measured 7 days after compression. In the acute compression study, NCV in the medium-dose group was significantly higher than that in the other groups during the compression period (P < 0.05). During the recovery period, there was no significant difference in NCV among groups. In the chronic compression study, NCV and blood flow in the cilostazol group were significantly higher than those in the control group (P < 0.05). Cilostazol improved NCV and blood flow to the cauda equina in this dog model. Cilostazol might be a potential agent to improve symptoms due to compression of cauda equina and/or cauda equina dysfunction.