Squamous cell papillomatosis of esophagus following placement of a self-expanding metal stent.

The esophageal self-expanding metal stent has gained widespread acceptance for the management of tracheoesophageal fistulas and the palliative management of malignant esophageal strictures. The complications associated with its use can be classified as either immediate or delayed. The most frequent delayed complications include tumor ingrowth, stent migration, reflux of gastric contents, bleeding, and perforation. This case report illustrates an otherwise unrecognized delayed complication of a self-expanding metal stent. Near complete ingrowth of the stent by squamous mucosal hyperplasia occurred within six weeks of the metal stent's placement. This finding supports the hypothesis that mucosal injury and regeneration underlies the etiology of esophageal squamous cell papilloma formation.

Tetrahydroisoquinolines (TIQs) do not act on opiate receptors in the guinea-pig ileum.

The myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum was stimulated with supra-maximal electrical field stimulation at 0.1 Hz. The contractile response was inhibited by salsolinol (1-300 microM) and tetrahydropapaveroline (THP) (3-30 micro M) but not by (cis)-3-carboxysalsolinol. S(-)-Salsolinol was more potent than R(+)-salsolinol. The inhibition by salsolinol and THP was unchanged by naloxone (up to 10 micro M). However, naloxone completely prevented the inhibition induced by normorphine, with a pA2 of 8.66. The results indicate that salsolinol and THP do not interact with opiate receptors in this preparation.

Acute and chronic effects of opiates on single neurons of the myenteric plexus.

Extracellular recordings were made from single neurons in the myenteric plexus of the guinea-pig ileum in vitro. Tissue was removed from morphine-naive guinea pigs and maintained in vitro for up to 24 hr; the firing rate of the neurons was reduced by opiate agonists and unaffected by opiate antagonists. Tissues were also removed from animals which had been pretreated with morphine during 3 days and placed into an in vitro solution which contained morphine. An increase in the concentration of morphine did not inhibit neuronal firing and naloxone caused a pronounced excitation of such cells. Cross-tolerance among different opiate agonists was apparent. In a third experiment, tissues were removed from morphine-naive guinea pigs and incubated in vitro for 24 hr in a solution which contained an opiate agonist. An increase in the concentration of agonist did not inhibit cell firing and opiate antagonists caused marked excitations of neurons incubated with morphine. Incubation with opiate agonists induced a much reduced sensitivity to the inhibitory effect of morphine on cell firing (tolerance) and also sensitized the cells to a marked excitatory effect of opiate antagonists (dependence) which was similar to the changes induced by in vivo opiate administration. The changes induced by morphine during 24 hr in vitro were not affected by the concomitant presence of sufficient lidocaine to prevent neuronal activity.

Inhibition of neuronal firing by opiates: evidence against the involvement of cyclic nucleotides.

1. Extracellular recordings were made in vitro from single neurones of the myenteric plexus of the guinea-pig ileum. 2. Neuronal firing was inhibited by morphine and normorphine (10 nM to 1 micrometer). Cyclic adenosine 3',5'-monophosphate (cyclic AMP) (100 micrometer to 1 mM) also inhibited the firing of the majority of the neurones. Prostaglandin E2 usually caused a short-lasting excitation of myenteric neurones and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine was usually without effect on firing rate. 3. The inhibition of neuronal firing by normorphine was unaffected by prior and/or concurrent administration of cyclic AMP, dibutyryl cyclic adenosine 3',5'-monophosphate, prostaglandin E2 or 3-isobutyl-1-methylxanthine. As these four treatments might be expected to elevate intracellular levels of cyclic AMP, the results lend no support to the notion that a reduction in intracellular cyclic AMP is essential to the inhibition of firing produced by morphine.