PREVENTION OF SPINAL-CORD ISCHEMIA BY SELECTIVE INTERCOSTAL ARTERIAL INFUSION OF PROSTAGLANDIN E-1

Purpose: A new protective method against the spinal cord ischemia that occurs during aortic clamping was investigated in dogs. Oxygenated bl ood containing prostaglandin E-1 (PGE(1)) was administered at the clam ped aortic segment, and the effect was evaluated by measurement of the sensory evoked spinal potential (SESP). Methods: In 30 dogs, a thorac otomy was made with dissection of the thoracic aorta. After intravenou s heparin (100 units/kg) was administered, the proximal and distal des cending thoracic aortas were cross-clamped for 60 minutes. Group A (n = 10) received oxygenated blood at the rate of 1.0 ml/kg/min. Groups B (n = 10) and C (n = 10) received oxygenated blood at the same rate, w ith PGE(1) at the dosage of 25 and 50 ng/kg/min, respectively. The inf usion was continuously administered throughout the entire period of is chemia. SESP was measured with epidural electrodes before clamping, 10 and 60 minutes after clamping, and 10 and 60 minutes after declamping . Neurologic outcome was assessed at 24 hours after the operation and graded according to the method of Tarlov. Results: There was no signif icant hemodynamic change in any group. At 60 minutes after clamping an d at 10 and 60 minutes after declamping, the amplitude of SESP was low er than that at preclamping in groups A and B (p < 0.05). At 60 minute s after clamping and at 10 and 60 minutes after declamping, the SESP w as more markedly decreased in group A compared with groups B and C. Re garding postoperative neurologic outcome, the dogs with SESP amplitude of more than 50% of the preclamping control value at 60 minutes after clamping showed neither paralysis nor paraplegia. Seven of nine dogs with less than 50% SESP amplitude showed neurogenic deficit. In a comp arison of groups A, B, and C, the Tarlov score for group A dogs was si gnificantly lower than that for group C dogs (p < 0.05). Conclusion: I n this model, PGE(1) administration at the rate of 50 ng/kg/min showed sufficient spinal cord protection against ischemia without a decrease in the blood pressure. Further studies are needed to determine the do se that will provide the maximal protective effect and to determine th e maximum duration of ischemia against which PGE(1) shows protective e ffects.