Colonic secretion studied in vitro in rats fed polyunsaturated fatty acids.

Recent studies primarily in man have shown that cod fish oil rich in polyunsaturated fatty acids (PUFA) are beneficial to certain inflammatory diseases such as ulcerative colitis. This study was undertaken to observe any change in intestinal secretion where the tissues have been treated with cod fish and sunflower oils. Male Sprague Dawley rats weighing 200 gms were fed omega-3 fatty acids for 50 days. Changes in colonic secretion (fed with PUFA) were studied in-vitro in an Ussing chamber. Rat colon which were not fed with PUFA served as controls. Basal intestinal short circuit in PUFA group were comparable with control group in stripped rat colon. The results showed significant high short circuit current in cod fish oil and sunflower oil treated tissues. When stripped colonic tissues (fed with PUFA) were stimulated by EC50 of carbachol, bradykinin and prostaglandin; there was no significant changes in Short circuit current. PGE2 and LTB4 levels were measured in rat colon fed with PUFA by using radioimmunoassay. Biochemical changes in PGE2 and LTB4 levels showed LTB4 were significantly raised in both cod fish oil group and sunflower oil group. This study reveals that intestinal permeability increases in the rat colon (fed with PUFA) as indicated by high short circuit current. The high levels of leukotriene in colonic tissues also explains the high basal short circuit current in the present study.

Carbachol potentiates cholera toxin-induced secretion in a colonic epithelial cell line (HT29-19A) and rat ileal mucosa in vitro.

Recent studies show that enteric nerves are involved in the action of cholera toxin, both in vivo and in vitro. The aim of this study was to investigate in vitro the influence of carbachol, a cholinergic agonist, on the action of cholera toxin. Cultured HT29-19A cell lines and rat ileal mucosa were used in an Ussing chamber for the measurement of short-circuit current induced by cholera toxin. Cyclic AMP was measured from HT29-19A cell lines by standard radio-immunoassay. Pre-treatment of the HT29-19A cell lines with carbachol potentiated cholera toxin-induced secretory response, and enhanced accumulation of cAMP. Carbachol also potentiated the cholera toxin-secretory response in the rat ileal mucosa, but only following pretreatment with the prostaglandin synthesis inhibitor, indomethacin. There was synergistic interaction between cholera toxin and cholinergic neurotransmitter carbachol on the intestinal epithelium. Cholinergic agonists may play a role in regulating the secretory response to the toxin. Such interaction is masked in the intact tissues in vitro due to the release of prostaglandins during isolation.