The acute effects of smokeless tobacco on transport and barrier function of buccal mucosa.

The acute effects of smokeless tobacco (ST) on buccal mucosal transport and barrier function were studied by means of in vivo and in vitro techniques. In humans, in vivo exposure to 0.5 g ST transiently increased the transmural electrical potential difference (PD). However, despite continued exposure, PD returned to baseline within 20 min. The mechanisms for these changes were explored by use of dog buccal mucosa mounted in Ussing chambers. Luminal exposure to a Ringer-extract of ST (EOST) increased PD and short-circuit current (Isc) and decreased electrical resistance (R), with changes reversible upon removal of EOST from the bath. Further, radioisotopic fluxes showed that the increase in Isc in EOST-exposed tissues was accompanied by increased absorption of electrolytes (Na, Cl, and other ions), and the decrease in R was accompanied by increased permeability to mannitol. Light microscopy of tissues exposed to EOST showed no morphological changes after exposure to 0.5 g of ST, but after exposure to 1.5-2.5 g of ST, dilated intercellular spaces were identified. Contact of aqueous media with ST led to the release of electrolytes and other soluble compounds into solution. To determine the effect of electrolyte release on buccal function, we exposed mucosae luminally to a solution with ion composition and/or osmolality similar to EOST or to one with an EOST previously dialyzed against Ringer. Solutions with similar ion composition and/or osmolarity changed PD, Isc, and R in a manner similar to EOST, while dialyzed-EOST had no effect. In addition, luminal nicotine produced effects different from EOST, decreasing PD and Isc and increasing R.(ABSTRACT TRUNCATED AT 250 WORDS)

Active electrolyte transport in mammalian buccal mucosa.

The transmural electrical potential difference (PD) was measured in vivo across the buccal mucosa of humans and experimental animals. Mean PD was -31 +/- 2 mV in humans, -34 +/- 2 mV in dogs, -39 +/- 2 mV in rabbits, and -18 +/- 1 mV in hamsters. The mechanisms responsible for this PD were explored in Ussing chambers using dog buccal mucosa. After equilibration, mean PD was -16 +/- 2 mV, short-circuit current (Isc) was 15 +/- 1 microA/cm2, and resistance was 1,090 +/- 100 omega.cm2, the latter indicating an electrically "tight" tissue. Fluxes of [14C]mannitol, a marker of paracellular permeability, varied directly with tissue conductance. The net fluxes of 22Na and 36Cl were +0.21 +/- 0.05 and -0.04 +/- 0.02 mueq/h.cm2, respectively, but only the Na+ flux differed significantly from zero. Isc was reduced by luminal amiloride, serosal ouabain, or by reducing luminal Na+ below 20 mM. This indicated that the Isc was determined primarily by active Na+ absorption and that Na+ traverses the apical membrane at least partly through amiloride-sensitive channels and exits across the basolateral membrane through Na+-K+-ATPase activity. We conclude that buccal mucosa is capable of active electrolyte transport and that this capacity contributes to generation of the buccal PD in vivo.

Multicenter trial of sucralfate suspension for the treatment of reflux esophagitis.

The efficacy of sucralfate suspension in the treatment of reflux esophagitis was assessed in a multicenter, randomized, double-blind, placebo-controlled trial. Sixty-eight patients with symptomatic and endoscopic esophagitis received either sucralfate suspension (n = 31) or liquid placebo (n = 37) for eight weeks. The two groups were comparable at entry with the exception that despite randomization, a disproportionately high number of patients with esophageal ulcers were assigned to receive sucralfate. After four and eight weeks of treatment, both groups had reduced heartburn frequency and severity, but there was no difference in improvement between sucralfate and placebo (p greater than 0.05). Endoscopic results after eight weeks of sucralfate treatment revealed complete healing in 36 percent (placebo, 35 percent) and improvement in an additional 45 percent (placebo, 24 percent). Although neither of these differences was significant, the percent of patients in whom healing or improvement occurred with sucralfate (81 percent) was greater than with placebo (59 percent) (p = 0.07). These data fail to establish that eight weeks of treatment with sucralfate suspension improves symptoms or heals lesions in reflux esophagitis at a rate significantly greater than placebo. However, the unequal distribution of patients with ulcers and the trend toward endoscopic improvement indicate that a potential beneficial effect of sucralfate suspension for the treatment of reflux esophagitis cannot be excluded.