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Although clinical instability is an in vivo problem, most spinal instability criteria are either subjective or are based on in vitro experiments. The authors performed an in vivo experiment using a canine model to study the natural history of spinal instability as a function of healing time up to 12 weeks. Three injuries were produced surgically: sham; laminectomy at C4; and bilateral facetectomy at C4-C5. Three 1.5-mm steel balls were implanted into C3 to C6 vertebrae at the time of surgery. Standardized functional flexion-extension stereoradiographs of the cervical spine were obtained before injury, immediately after injury and at 0.5, 1, 1.5, 2, 3, 4, 5, 6, 7.5, 9, and 12 weeks postinjury and immediately after killing the animals. In general, the authors found decreased ranges of motion (ROM) at the C4-C5 level, compared with the pre-injury values, for all injuries, but most significantly for the facetectomy. The maximum decrease occurred between 0 and 0.5 weeks postinjury. Between 2 and 12 weeks, there was recovery in the ROM, especially for the two less severe injuries. The changes in the ROM at each spinal level were explained by simultaneous presence of a destabilizing factor, caused by the three different injuries with the sham as the least and the facetectomy as the most destabilizing injury, and a stabilizing mechanism of muscle spasm in the beginning and of healing and other adaptive responses in the late phase after injury. Because of the significant differences between the canine model and the human cervical spine, the present findings should be extrapolated to the human situation with caution.

We examined the effects of metabolic acidosis in vivo and reduced bath and luminal pH in vitro on total NH3 (NH3 + NH+4) production rates by isolated mouse proximal tubule segments. Midproximal tubule segments were obtained from mice with NH4Cl-induced metabolic acidosis and from nonacidotic controls. The segments were perfused with modified Krebs-Ringer bicarbonate (KRB) buffer, incubated in KRB buffer containing 0.5 mM L-glutamine and 1.0 mM sodium acetate, and gassed with 95% O2 and 5% CO2. Isolated unperfused and perfused proximal tubules from acidotic mice produced total NH3 at higher rates than corresponding tubules from nonacidotic mice. Perfusion of the tubular lumen stimulated total NH3 production by tubules from both acidotic and nonacidotic mice. In contrast, lowering the bath pH to 7.0 by lowering the HCO3- concentration increased total NH3 production rates by tubules from nonacidotic mice but not by tubules from acidotic mice. Reducing the HCO3- concentration of the bath buffer to 10 mM while maintaining a pH of 7.4 had no significant effect on total NH3 production by tubules from nonacidotic mice. Lowering the luminal fluid pH by reducing the perfusate HCO-3 from 25 mM to 10, 5, or 1.2 mM while maintaining a bath pH of 7.4 lowered collected luminal fluid pH but had no effect on total NH3 production by proximal tubules from nonacidotic mice. These observations demonstrated that metabolic acidosis in vivo stimulated total NH3 production in isolated mouse proximal tubule segments and that low peritubular pH and HCO-3 stimulated total NH3 production by proximal tubule segments from nonacidotic mice in vitro.