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  • Title: Spinal cord blood flow and pathophysiological changes after transient spinal cord ischemia in cats.
    Author: Yamada T, Morimoto T, Nakase H, Hirabayashi H, Hiramatsu K, Sakaki T.
    Journal: Neurosurgery; 1998 Mar; 42(3):626-34. PubMed ID: 9526997.
    Abstract:
    OBJECTIVE: The goal was to study the hemodynamics and regional pathophysiological changes in the spinal cord after transient vascular occlusion in cats. METHODS: We measured spinal cord blood flow (SCBF) continuously in the lumbar region with a laser-doppler flowmeter, before, during, and after spinal cord ischemia induced by balloon occlusion of the thoracic aorta, in 24 cats (divided into three groups) and simultaneously recorded the evoked spinal cord potentials (ESPs). In each group (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 ESPs decreased 10 minutes and disappeared 20 minutes after occlusion. SCBF increased to as much as 2 times the control values after reperfusion 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 the 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, hypoperfusion after recirculation, irreversible amplitude changes in ESPs, 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 have an important role in the development of secondary spinal cord ischemia, resulting in severe neurological dysfunction. This observation suggested the possibility of therapeutic modification of the secondary processes inducing hypoperfusion after spinal ischemia.
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