Akademik Veri Yönetim Sistemi
Turk Anesteziyoloji ve Reanimasyon, cilt.24, sa.9, ss.388-393, 1996 (Scopus)
The effect of pentoxifylline (PTX), an agent known to inhibit in vitro neutrophil activation and improve recovery after cerebral ischemia in animals, was investigated on spinal cord protection. Twenty four New Zealand white rabbits were used for spinal cord ischemia models. Infrarenal aortic occlusion devices were placed. After 48 hours, 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. Histological analysis of the spinal cords was carried out immediately after acute paraplegia or within 24 hours after development of delayed paraplegia. During the aortic occlusion, the distal aortic pressures were the same in both groups. At the 72nd hour, the scores were not different in both groups (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 (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. We conclude 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 do not seem to change the outcome.