Purpose: The purpose of this study was to investigate whether or not 5-minute segmental intraaortic perfusion of prostaglandin E1 (PGE1) in the preischemic period has a protective effect against spinal cord ischemia during aortic cross clamping.
Methods: The rabbits were divided into two groups. In group A (n = 6), the infrarenal aorta was segmentally cross clamped and the segment was perfused for 5 minutes with blood and saline solution at first. The aorta was kept cross clamped without perfusion for a subsequent 20 minutes. In group B (n = 6), the infrarenal aorta was segmentally cross clamped and the segment was perfused for 5 minutes with blood and saline solution containing PGE1 of 100 ng/kg/min at first. The aorta was kept cross clamped without perfusion for a subsequent 20 minutes. After the aorta was declamped, the experimental animals recovered from the anesthesia. Twenty-four and 48 hours after the operation, the hind limb function was estimated with Tarlov's grade. Then, the animals were killed for pathologic study.
Results: The systolic arterial pressures measured at the left common carotid artery through the experiment were not significantly different between the two groups. The perfusion of the aortic segment between the proximal and distal clamp was nonpulsatile. The perfusion pressures of the aortic segments at 5 minutes after aortic cross clamping were 29 +/- 6 mm Hg and 33 +/- 6 mm Hg in groups A and B, respectively. No significant differences were seen between the two groups. In group A, the hind limb functions evaluated with Tarlov's grade after 24 hours and 48 hours were 0 to 3 (1.5 +/- 1.4) and 0 to 3 (1.3 +/- 1.4), respectively. In group B, these were 3 to 4 (3.5 +/- 0.5) and 3 to 4 (3.7 +/- 0.5), respectively. A significant difference was seen between the two groups (P <.05). In the ventral horn of the L5, L6, and L7 segments, large motor neurons that seemed viable were more preserved in group B than in group A.
Conclusion: Segmental intraaortic perfusion of PGE1 in the preischemic period reduced neurologic damage of spinal cord ischemia.