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People addicted to opium rarely develop intra-abdominal adhesions after abdominal surgery. We aimed to evaluate the effect of opium or morphine on preventing postoperative adhesions in rats. Sixty-three rats were randomly divided into a control group, opium-addicted group, and morphine-addicted group in a double-blind study. Drug dependency was checked by using naloxone. Animals were then operated on and the cecum was abraded. At reoperation 3 weeks later the magnitude of adhesions was evaluated by a scoring system. There was a significant difference between the control, opium-addicted, and morphine-addicted groups with regard to the length (P < .001), thickness (P < .05), and severity of adhesions (P < .05). Opium or morphine reduces the severity of postoperative adhesions. Elucidation of the opioid receptor(s) involved in this process would enable the use of selective ligands and offer a pharmacologic strategy in preventing adhesion formation.

The effect of cholera toxin on small intestinal capillary function, utilizing the Evans blue dye method, was analyzed. The modulatory influence of plasma-derived or recombinant human antisecretory factor on this variable was also investigated. Male Sprague-Dawley rats were briefly anesthetized with ether, and a jejunal loop was constructed that was challenged for 90 min with phosphate-buffered saline or cholera toxin. Five minutes prior to death, the rats received an intravenous injection of Evans blue. The tissue content of dye in the loop was quantitated spectrophotometrically or demonstrated histochemically. Cholera toxin increased the recovery of Evans blue; extravasation of the dye was prominent in the top of the villi, while the crypts were spared. It is suggested that the toxin caused increased transcapillary permeation of albumin in a heterogenous fashion in the gut wall. This effect of the toxin was prevented by pretreatment with the antisecretory factor.

In the present study, we addressed the problem whether sympathoadrenal mechanisms could influence the paracellular permeation of macromolecules from the lumen to the lamina propria of the small intestine. Experiments were conducted with rats that were anesthetized with ether for 10-20 min, during which time laparotomy was performed and six consecutive loops (each of 5 cm length) of the jejunum were prepared. A 3% solution of the azo dye, Evans blue (EB; MW 960.83) in phosphate-buffered saline, was instilled into each loop at a volume of 0.3 ml, this compound serving as a marker for tight junctional permeability. Thereafter, the abdomen was closed and the rats were allowed to wake up, but were killed after 60 min. The loops were dissected, opened, and rinsed with acetylcysteine in order to remove the adherent mucus layer. Each loop was weighed and incubated with formamide for 24 hr to elute the amount of EB absorbed, which was quantitated spectrophotometrically. In the control situation, the uptake was homogenous along the loops. beta-Adrenoceptor-blocking, or -stimulating agents could influence the uptake considerably. The data obtained could indicate that noradrenergic nerves, via an activation of beta 2-adrenoceptors, may cause an increase of tight junction permeability for macromolecules, but circulatory mechanisms also must be taken into account in order to explain the observed effects.