[abstract] SPINAL CORD DYSFUNCTION AND PATHOLOGY FOLLOWING ARTERIAL GAS EMBOLISM.

Abstract

Four anesthetized canines were given embolic air in the mid-thoracic aorta at a rate of 1.0 ml/min via PE-IO tubing with an internal diameter of 0.28 mm. Embolization was continued for a maximum of 30 min or less if spinal somatosensory evoked potentials (SSEP) recorded at the T13/L1 and 1.1/1,2 levels became isoelectric. Perfusion fixation of the spinal cord using Karnovsky's solution was carried out four hours after completion of embolization. Serial sections of the cord distal to T13 were subsequently mounted in epoxy-resin and cut into 2 micron sections, which were then stained with a universal stain solution for examination by light microscopy. Light microscopy showed gross disruption of the gray matter with acute edema. In marked contrast, there was almost total sparing of the white matter. The overall appearance bore no resemblance to that of canine spinal cords perfusion fixed four hours after induced decompression sickness severe enough to produce isoelectric SSEP. In particular, the selective sparing of the white matter contrasts with the white matter lesions described as typical of decompression sickness in a variety of species. It is concluded that arterial gas emboli of the size used in this experiment play no major part in the creation of the spinal cord pathology associated with decompression sickness. (Supported by NMRDC Work Unit M0099.01C-1053)