Search

Spinal cord Na, K, Ca, and H2O changes were measured 6 h after graded contusion injuries in 40 Sprague-Dawley rats. A 10 g weight was dropped 1.25 cm (n = 6), 2.5 cm (n = 7), 5.0 cm (n = 6), or 7.5 cm (n = 7) onto the thoracic spinal cord of 26 rats. An additional 10 rats served as laminectomy controls and 4 rats were unoperated controls. At 6 h after surgery or injury, the spinal cords were rapidly cut into 4 mm segments, weighed to obtain tissue wet weights (W), dried for 14-16 h at 97 degrees C in a vacuum oven (30 mmHg), and reweighed for tissue dry weights (D). Water concentrations ([H2O]d) were estimated from (W-D)/D in units of ml/g D. Ionic concentrations ([Na]d, [K]d, and [Ca]d) of the tissue samples were measured by atomic absorption spectroscopy with units of mumol/g D. Ionic shifts (delta [Na]d, delta [K]d, delta [Ca]d) were calculated by subtracting laminectomy control values from those measured in injured cords. Laminectomy alone significantly increased [Na]d and [H2O]d compared to unoperated controls. Mean +/- standard deviations of [H2O]d, [Na]d, [K]d, and [Ca]d were, respectively, 1.95 +/- 0.07, 182.6 +/- 5.9, 277.2 +/- 11.8, and 12.1 +/- 1.4 in unoperated controls; 2.12 +/- 0.08, 238.6 +/- 9.2, 277.8 +/- 9.2, and 11.7 +/- 1.1 in laminectomy controls. At the impact site, [K]d fell by 14-37% and [H2O]d rose by 14-24%, [Na]d by 13-64%, and [Ca]d by 65-137% of laminectomy control values. delta [Na]d, delta [K]d, and delta [Ca]d correlated linearly with impact velocities; [Ca]d increased by 1.0% per cm/sec (r = 0.995, p less than 0.005), [Na]d increased 0.67% per cm/sec (r = 0.950, p less than 0.01), and [K]d decreased 0.34% per cm/sec (r = 0.964, p less than 0.01). Neither delta [H2O] nor delta [Na]d + delta [K]d consistently predicted impact velocity. [Na]d + [K]d correlated with [H2O]d with a slope of 177.4 mumol/ml (r = 0.697, p less than 0.005). Since Na and K constitute greater than 95% of tissue inorganic ions, the slope approximates net ionic shift per ml of water entry or the ionic osmolarity of edema fluid. These results indicate that increasing contusions produce graded ionic shifts and that edema does not predict contusion severity. These data support our hypothesis that net ionic shifts cause edema in injured spinal cords.

Three related hypotheses are proposed. (1) Many simple viruses disassemble in the act of crossing a membrane, drawing energy from ionic disequilibria across the membrane. (2) Many of the metabolic changes early in virus infection are due to altered ion fluxes across membranes and the consequently altered ion concentrations in cytoplasm. (3) The crucial determinant of the transformed phenotype is also a change in ion concentrations. Ca2+ ions may play a major role in these effects.