Electron Microscopy of Cat Spinal Cord Subject to Circulatory Arrest and Deep Local Hypothermia (15 C)

Abstract

Circulatory arrest to the lumbar spinal cord of adult cat was produced by occlusion of the descending aorta and concurrent arterial hypotension. Local hypothermia of the cord was induced by paraffin oil at 5 C, which was circulated over the exposed surface of the cord, using the laminectomy wound as a trough. Intramedullary temperature was 15 C at a depth of 5 mm. In 10 control animals oil at 37 or 5 C was circulated over the exposed cords (normal-normothermic and normal-hypothermic controls with 1 and 2 hours hypothermia). Three animals had circulatory arrest and recirculation in normothermia (ischemic-normothermic) and 3 in hypothermia (ischemic-simultaneous hypothermia). Three had circulatory arrest and 15 minutes of recirculation in normothermia followed by 1 hour of hypothermia (ischemic-delayed hypothermia). The medial and lateral portions of the anterior gray horns of the last lumbar spinal segment were studied in the light and electron microscopes. Ischemic-normothermic tissue showed 20% shrinkage in mean areas of neuronal perikarya and massive “watery” swelling of astrocytic cell bodies and processes. Within neuronal perikarya and dendrites, cytoplasm increased in electron density, ribosomes dispersed, Golgi apparatus swelled and mitochondria swelled with loss of matrix density and disruption of cristae. Axons and axon terminals did not increase in size, but mitochondria within these structures doubled in size without loss of matrix density or change in pattern of cristae. Synaptic vesicles were no longer uniform in size, and they were clumped away from the synaptic cleft and diminished in number. Lysosomes were unchanged in appearance and size. Mitochondria of astrocytes underwent approximately fourfold enlargement without loss of matrix density or pattern of cristae. Bundles of astrocytic microfilaments were fragmented, spread apart and diminished in quantity. Oligodendroglia and endothelial cells were unchanged. Normal-hypothermic animals were similar to normal-normothermic except for clefts in rough endoplasmic reticulum of neurons and dendrites. These clefts were formed by a separation of the cisternal membrane from the adjacent row of ribosomal rosettes. Ischemic-simultaneous hypothermia animals had findings identical to normal-hypothermic animals. Ischemic-delayed hypothermia animals were similar to ischemic-normothermic animals except for less swelling of astrocytic processes, greater swelling of astrocytic mitochondria and less alteration of microfilaments. The findings show that ischemia in normothermia brings about alterations in virtually every organelle of the neurronal perikaryon except the lysosome. Simultaneous hypothermia in ischemia prevents the protean alterations of ischemia, whereas hypothermia delayed until after the ischemic episode only slightly modifies the cellular lesions found in ischemic-normothermic animals.

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