SPINAL-CORD BLOOD-FLOW AND PATHOPHYSIOLOGICAL CHANGES AFTER TRANSIENTSPINAL-CORD ISCHEMIA IN CATS

OBJECTIVE: The goal was to study the hemodynamics and regional pathoph ysiological changes in the spinal cord after transient vascular occlus ion in cats. METHODS: We measured spinal cord blood flow (SCBF) contin uously in the lumbar region with a laser-doppler flowmeter, before, du ring, and after spinal cord ischemia induced by balloon occlusion of t he thoracic aorta, in 24 cats (divided into three groups) and simultan eously recorded the evoked spinal cord potentials (ESPs). In each grou p (n = 8), 10-, 20-, and 30-minute ischemic loading was performed. All animals were evaluated neurologically 36 hours later, and then their spinal cords were examined histologically. RESULTS: The amplitude of E SPs decreased 10 minutes and disappeared 20 minutes after occlusion. S CBF increased to as much as 2 times the control values after reperfusi on and decreased gradually in all groups. Then, in all animals in the 10-minute group and six animals in the 20-minute group, SCBF returned to the control values, which were subsequently maintained throughout t he experiment, and ESPs returned to normal patterns within 1 hour. For all animals in the 30-minute group and two in the 20-minute group, hy poperfusion after recirculation, irreversible amplitude changes in ESP s, postischemic paraparesis, and pathological ischemic changes in the lower thoracic and lumbar spinal segments were recognized. CONCLUSION: Our results showed that >20-minute occlusion of the thoracic aorta in cats resulted in irreversible spinal perfusion disorders and that the monitoring of SCBF and ESPs could be useful for predicting potential neurological deficits. Furthermore, postischemic hypoperfusion may hav e an important role in the development of secondary spinal cord ischem ia, resulting in severe neurological dysfunction. This observation sug gested the possibility of therapeutic modification of the secondary pr ocesses inducing hypoperfusion after spinal ischemia.