European Journal of Cardio-Thoracic Surgery, Vol 12, 648-653, Copyright © 1997 by European Association for Cardio-thoracic Surgery
Evaluation of pentoxifylline in experimental spinal cord ischemia
A Turkoz, R Turkoz, K Yorukoglu, U Onat, E Sagyroglu and M Sagban
Department of Anesthesiology, Dokuz Eylul University Hospital, Izmir, Turkey.
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 in vitro 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) were given PTX 40 mg/kg i.v. 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.
