EFFECT OF PROXIMAL ARTERIAL PERFUSION-PRESSURE ON FUNCTION, SPINAL-CORD BLOOD-FLOW, AND HISTOPATHOLOGIC CHANGES AFTER INCREASING INTERVALS OF AORTIC OCCLUSION IN THE RAT

Background and Purpose Cross-clamping of the thoracic aorta results in spinal cord ischemia and prominent systemic hy hypertension. Using a rat model of transient spinal cord ischemia, we examined the effects o f manipulation of proximal aortic blood pressure on spinal cord blood flow (SCBF), neurological dysfunction, and changes in spinal histopath ology after increasing intervals of aortic occlusion. Methods Aortic o cclusion was induced by the inflation of a 2F Fogarty catheter placed into the thoracic aorta in rats anesthetized with halothane (1.5%). A tail artery was cannulated to monitor distal arterial pressure (DAP). To measure SCBF, a laser probe was implanted into the epidural space o f the L-2 vertebra. To manipulate proximal arterial pressure (PAP), th e left carotid artery was cannulated with a 20-gauge polytetrafluoroet hylene catheter to permit blood withdrawal and infusion from a periphe ral reservoir during aortic occlusion. In a survey study, spinal cord ischemia was induced in single animals at intervals of 6, 10, 15, 30, or 40 minutes with PAP controlled at 40, 60, 80, and 110 to 120 mm Hg. In a second series, ischemia was induced in groups of animals for 0, 6, 8, 10, and 12 minutes with PAP controlled at 40 mm Hg. After ischem ia the animals survived for 2 to 3 days. During this recovery period, neurological functions were evaluated, followed by quantitative histop athology of the spinal cord. Results Under normal conditions, cross-cl amping yields an acute proximal hypertension (125 to 135 mm Hg), a fal l of DAP to 15 to 22 mm Hg, and a decrease in SCBF to 7% to 11% of bas eline values. With the use of the external reservoir, proximal hyperte nsion could be abolished and the PAP maintained at target pressures. I n these studies a typical syndrome of tactile allodynia, spastic parap legia, and necrotic changes affecting the central part of the gray mat ter after 24 to 48 hours of reperfusion was observed at the following combinations of ischemic intervals and PAP values: >10 minutes/40 mm H g; >12 minutes/60 mm Hg; >16 minutes/80 mm Hg; and >30 minutes/uncontr olled. Lowering PAP resulted in a corresponding decrease in residual S CBF. Systematic studies at a PAP of 40 mm Hg at occlusion intervals of 6, 8, 10, and 12 minutes revealed that 100% of rats were paraplegic a fter 10- and 12-minute ischemia, and these rats showed corresponding s igns of spinal histopathology. Conclusions The present study shows tha t systemic intraischemic hypotension (40 mm Hg) significantly potentia tes neurological dysfunction after transient aortic occlusion. The mec hanism of the observed effect may include elimination of collateral fl ow during aortic occlusion and/or consequent potentiation of hypoperfu sion during reperfusion. These data indicate that PAP during occlusion should be monitored and/or controlled because it is a critical variab le in the determination of outcome in this model of spinal cord ischem ia.