A variety of seemingly diverse pain syndromes are characterized by movement-induced pain radiating in the distribution of a peripheral nerve or nerve root. This could be explained by the induction of ectopic mechanical sensitivity in intact sensory axons. Here we show that inflammation led to mechanical sensitivity of the axons of a subset of mechanically sensitive primary sensory neurons. Dorsal root recordings were made from 194 mechanically sensitive neurons that innervated deep and cutaneous structures and had C, Adelta, and Aalphabeta conduction velocities. No axons of any category were mechanically sensitive in control experiments. However, the axons of neurons innervating deep structures and having C- or Adelta-conduction velocities became mechanically sensitive during the neuritis, and also exhibited an increased incidence of spontaneous discharge. The incidence of mechanical sensitivity followed a distinct time course. In some cases, paw withdrawal thresholds were obtained after neuritis induction. The time course of the resultant hypersensitivity was not directly related to the time course of the axonal mechanical sensitivity. Ectopic axonal mechanical sensitivity could explain some types of radiating, nerve-related pain coexisting with diseases of seemingly diverse etiologies.
Colons of male Sprague-Dawley rats were perfused, in situ, with ammonium (NH4+) or sodium (Na+) and acetate (CH3COO-) or chloride (Cl-) to determine the effects of the cations and anions or their interactions on the colon mucosa. Solutions simulating ileal fluid were delivered at 0.4 mL/min at 38 degrees C via cannulae inserted at the cecal-colonic junction. Effluents were collected by cannulae inserted in the anus. In the first experiment, perfusion with the control solution or with the control solution having 35 mmol/L NaCl replaced by equimolar amounts of ammonium acetate, ammonium chloride or sodium acetate showed that only ammonium-containing solutions caused histological damage, loss of mucus, and significant losses of carbohydrate and DNA (P less than 0.05). The losses of carbohydrate and DNA expressed in microgram.cm-1.30 min-1 were as follows: control, 13.4 and 1.0; ammonium acetate, 31.8 and 1.6; sodium acetate, 16.0 and 0.6; ammonium chloride, 24.1 and 1.3, respectively. In the second experiment, perfusion with control fluid containing 35 or 70 mmol/L ammonium acetate at pH 6.8, 7.4 or 8.0 increased carbohydrate and DNA losses into the effluents compared with the pretest period (P less than 0.05), without significant effects related to influent pH. These studies are consistent with the concept that the life span of colon cells is shortened by concentrations of ammonia found in the colon under normal conditions and that ammonia enhances cell proliferation in the colon mucosa.
Mature male Sprague-Dawley rats were assigned to a 3 x 3 factorial experiment in which they were fed AIN-76A diets supplying 8, 16 and 32% of energy as protein and 12, 24 and 48% of energy as fat. During the 5 mo of feeding, 10 in vivo measurements of intracolonic pH were recorded on each rat with a flexible electrode. The pH ranged from 7.8 to 8.0 near the anus and declined to 7.4 to 7.5 at 12 cm from the anus. The mean percentages of dry matter in the contents of the colon, divided into three approximately equal segments, were as follows: proximal colon, 35; middle colon, 45; distal colon, 58. Ammonia concentrations in luminal fluid rose significantly with higher protein intake in the cecum, proximal colon and distal colon. The concentrations in the distal colon ranged from 39 to 74 mmol/L, depending upon protein intake. Thymidine incorporation by distal colon mucosal cells was higher in rats fed 32% of energy as protein and 48% of energy as fat compared with rats fed 8% of energy as protein and 12% as fat. The evidence suggests that increased intestinal cell proliferation in rats fed the high protein, high fat diet was due to greater concentrations of ammonia in the large intestine resulting from the high protein intake and greater concentrations of non-ionized ammonia resulting from the higher pH associated with increased fat intake. The actual determinations and calculations of ionized to non-ionized ammonia concentrations were compatible with the assumption that the large intestinal cells absorbed more ammonia at higher fat intakes.
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