Abstract

Spinal cord damage is an uncommon but disastrous complication of aortography. The development of less neurotoxic opaque media, and especially the replacement of acetrizoate by diatrizoate arid iothalamate salts, has reduced but not completely eliminated this problem. Although there is some dispute about the pathogenesis of cord injury (whether a direct chemotoxic (1, 10–12) or a hyperosmotic (7) effect of the contrast agent), most authorities agree on the mechanism of the injury—too much concentrated opaque medium perfusing the spinal cord capillary bed. Therefore, any factor tending to increase the flow to or prolong the transit time through the cord during aortography increases risk of serious damage. Margolis and his associates (1, 12) were the first to demonstrate the striking enhancement of spinal cord toxicity when a pressor amine is administered prior to aortography. Under these circumstances, both diatrizoate and iothalamate salts in conventional doses may produce extensive cord damage with paraplegia in dogs. These authors postulated that this enhancement of neurotoxicity was the result of the differential reactivity of the splanchnic∕somatic vascular beds and the vessels of the spinal cord to vasoactive substances. Neural vasculature in general responds less vigorously to the hypertensive effects of vasopressor agents (16); therefore, a small dose of levarterenol prior to aortography would divert opaque media away from the constricted visceral and peripheral circulations into the vascular bed of the cord. Margolis et al. (1, 12) illustrated prolonged hold-up of the contrast bolus in the aorta following levarterenol infusions and, with electromagnetic flowmeters, measured an actual increased flow in the lumbar segmental arteries from which, in the dog, blood supply to the lower cord arises (9, 17). In addition, extensive cord lesions were demonstrated histologically after administration of extremely small doses of contrast medium (as little as 2 ml of Urokon in a 15–20 lb. dog). Winkler and Kahn (18) also reported an increased incidence of paraplegia in dogs when aortography follows epinephrine infusion. All this evidence indicates that vasopressor amines, because of the differential reactivity of neural and extraneural vasculature, will tend to drive the bulk of an intra-aortic injection toward the spinal cord. Actual perfusion of the cord vascular bed with an increased volume of opaque medium following vasopressor infusions has not, however, been arteriographically demonstrated. We therefore undertook an investigation of this phenomenon in an attempt to visualize the postulated shunt as well as to evaluate factors that might influence cord perfusion and cord toxicity during aortography. Materials and Methods Sixteen monkeys (Macaca mulatta) weighing 3–6 kg were used in these studies.

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