Biomedical subjects
Publications and source records attributed to D L Dean.
Morphologic evidence for calcium salts within the brains of severely stressed neonates at autopsy correlated to the mean daily parenteral dose of calcium gluconate (P less than 0.01). Survival analysis indicated that parenteral administration of calcium contributed a negative effect to predicted survival (P less than 0.05).
Parenteral calcium may augment the degree of calcification within brains of human neonates (p less than 0.01). This observation is supported by histochemistry, atomic absorption of ashed brain, selected area diffraction, and energy dispersive microanalysis. Survival analysis indicates that a standard replacement dose may have an adverse effect of severely stressed neonates (p less than 0.01). Nuclei within the optic-tract, circumferential pons and temporal lobe showed calcium salt deposits before other cytologic evidence of necrosis was discernible. Most calcification occurred in regions of ongoing necrosis primarily in the neuropil. But Purkinje cell and supraoptic neurons and apparent neurons from the fascia dentata, Ammon's Horn, were densely calcified in several brains. In those infants surviving longer periods both the neuropil and nuclei of glial scar stained for calcium salts.
Selective axonal calcification has been consistently observed in experimental spinal cord trauma in laboratory animals as well as in human spinal cord injury. A hypothesis of calcium influx resulting in activation of proteolytic and/or lipolytic enzymes has been proposed as a major mechanism of nerve fiber degeneration. The current study was undertaken to determine the effects of calcium influx into nontraumatized spinal cord tissue, utilizing 10 per cent calcium chloride at a pH of 7.4 slowly dripped onto the dorsal surface of the surgically exposed spinal cord of adult male Sprague-Dawley rats. Controls consisted of animals similarly treated with solutions of sodium chloride, magnesium chloride, and potassium chloride at the same pH and osmolarity. Sham-operated and normal animals were also observed. The experimental animals that received calcium chloride consistently developed paraplegia that was evident within 24 hours after treatment. The initial spinal cord lesion consisted of discrete areas of spongiosis in posterior and lateral columns in the segment beneath the application of calcium. The spongiosis progressed in severity and was accompanied or followed by necrosis. The gray matter was relatively spared; however, the posterior horns became consistently necrotic. Calcium was observed histochemically in the areas of spongiosis/necrosis but not in spared areas. Although the topography of the calcium-induced myelopathy differs from that of spinal cord injury, the progression of the clinical and pathologic changes is consistent with the calcium-mediated hypothesis of necrosis in the latter.
Explore the source record for details and available documents.