Objective: Despite the advance of anesthesia and surgery, postoperative neurological dysfunction has remained a challenging problem after descending and thoracoabdominal aortic surgery. The pathophysiology of early and especially late paraplegia is not clearly understood. The effect of pentoxifylline (PTX), an agent known to inhibit invitro neutrophil activation and improve recovery after cerebral ischemia in animals, was investigated on spinal cord protection. Methods: Twenty four New Zealand white rabbits were used for spinal cord ischemia models. Infrarenal aortic occlusion devices were placed. After 48 h, the rabbits were randomly taken for study. The PTX groups (n = 12) was given PTX 40 mg/kg IV bolus followed by 0.2 mg/kg/min infusion. The control (CT) group (n = 12) received normal saline. Two groups underwent temporary (20-24 min) spinal cord ischemia in a conscious state. After the operation, the spinal cord function was assessed at 6, 12, 24, 48 and 72 h by the scale (score of 5 = normal hop, score of 0 = no movement). Histological analysis of the spinal cords was carried out immediately after acute paraplegia or within 24 h after development of delayed paraplegia. Results: During the aortic occlusion, the distal aortic pressures were the same in both groups (PTX group: 14.92 +/- 3.78 mmHg; CT group: 17.42 +/- 3.2 mmHg). At the 72nd h, the scores were not different in the PTX group (1.58 +/- 2.11) and in the CT group (0.83 +/- 1.95) (P = 0.817). Acute paraplegia developed in 3 rabbits (25%) of each group. Delayed paraplegia was observed in 6 rabbits (50%) in the PTX group and 7 rabbits (58%) in the CT group. On morphological examination on the spinal cords. ischemic changes were observed in both groups. Although neutrophil leukocytes were noted in the control group with acute paraplegia and macrophage infiltration was noted in the control group with delayed paraplegia, there was not any leukocyte or macrophage sequestration in the PTX group. Conclusions: Neurological deficits after spinal cord ischemic/reperfusion injury were not directly responsible for blood-originated phagocytic cells and the inhibition of this type of cell function did not change the outcome. (C) 1997 Elsevier Science B.V.