The effect of O-(beta-hydroxyethyl)-rutosides (Venoruton) on function and structure of the motor anterior-horn cells of the lumbar spinal cord was investigated under conditions of ischemia in the rabbit. The determination of the functional parameters of the ganglion cells, such as maximal function time (Fm), disappearance time (SFm), relative efficiency (La), and regeneration expenditure (Ea) revealed that 50 mg/kg of Venoruton injected prior to repeated aortic occlusion of short duration (occlusion time A = Fm and A = 2 Fm, respectively) caused the efficiency of the anterior-horn cells to be decreased. Both qualitative and quantitative analysis of the mitochondrial structure after prolonged aortic occlusion (15-25 min) revealed that after prior injection of Venoruton irreversible structural changes in the mitochondrial membranes of the ischemic area in the spinal cord occurred after aortic occlusion of 15 min duration. In the untreated controls such changes were not observed before 20 min of occlusion. The mitochondrial structure of the non-ischemic area in the spinal cord was found to be undamaged, however, in both controls and experimental animals. Venoruton given after prolonged aortic occlusion resulted in less pronounced structural changes of the mitochondria in the ischemic area of the experimental animals than those found in the untreated controls; paralysis of the hind extremities was found to occur only after prolonged occlusion (25 min), whereas in the controls such changes were already observed after 20 min of occlusion. Since no ultrastructural changes in the ganglion cells of the non-ischemic area in the in the lumbar spinal cord were observed after application of Venoruton, it is assumed that the decreased efficiency of the motor anterior-horn cells found in the ischemic area when Venoruton had been injected before the aortic occlusion may be due to reactions of the cell that only occur when the blood supply has been completely cut off and Venoruton is present at the same time.