EXPERIMENTAL DELAYED POSTISCHEMIC SPINAL-CORD HYPOPERFUSION AFTER AORTIC CROSS-CLAMPING

Background: As in the brain, recent evidence has suggested a defect in the microcirculation during the reperfusion period after spinal cord ischemia. This investigation was undertaken in order to delineate bloo d flow dynamics in the postischemic spinal cord of the rat. Methods: M ale Sprague-Dawley rats underwent cross-clamping of the aorta and subc lavian arteries (XC) for 11 minutes. Spinal cord blood flow (SCBF) was measured by autoradiography in the gray and white matter of cervical (Ce), thoracic (Th) and lumbar (Lu) regions during XC, 1 h, 6 h and 24 h (XC n = 8, 1 h n = 9, 6 h n = 9, and 24 h n = 11, groups) after XC. Control groups underwent surgical manipulations and SCBF measurement but no XC (Sham 1, n = 8), or clamping of the subclavian arteries only (Sham 2, n = 8). Results: In Ce cord, there was no difference between SCBF of 1 h, 6 h, 24 h and Sham 1. In Th cord, SCBF was reduced durin g XC (P < 0.003 vs. Sham 2), 1 h, 6 h (P < 0.04 and P < 0.01 vs. Sham 1). In Lu cord, SCBF was not detectable in XC, and depressed in 1 h (P < 0.003) and 6 h (P < 0.003). There was no difference between 24 h an d Sham 1 in Ce, Th, and Lu cords. Conclusions: The study demonstrated a period of delayed postischemic hypoperfusion in the white and gray m atter of Th and Lu cord segments lasting 6 h after XC. The phenomenon may play an important role in the ultimate fate of neural elements wit h borderline viability after ischemic injury.