Studies on hydragogue drugs: light and electron microscopic examination of the isolated rat colonic mucosa exposed to deoxycholic acid and synthetic surfactants.

Sacs of the stripped and everted, isolated descending rat colon were incubated for 2 hours in presence of the following surfactants at the mucosal side: Dodecylsulphate (DDS), dioctylsulphosuccinate (DOSS), cetrimonium bromide (CTMAB), Triton X100 and deoxycholic acid (DOC). After tissue fixation, the sacs were processed for light microscopy (LM) and for scanning (SEM) and transmission (TEM) electron microscopy. All three methods revealed that DOSS (1.3 X 10(-4) and 2.6 X 10(-4) mol/l, CTMAB (5 X 10(-5) and 1 X 10(-4) ) and Triton (2 X 10(-5), 5 X 10(-5) and 1 X 10(-4) ) caused only minor or moderate changes compared to parallel controls, as did also DDS at 1 X 10(-5) and 2 X 10(-5) mol/l. DDS at 2 X 10(-4) and 4 X 10(-4) mol/l and DOC at 1.5 X 10(-4) and 3 X 10(-4) mol/l caused more prominent changes. LM showed swollen, vacuolated cells with pycnotic nuclei; many of these cells seemed to be extruded. According to SEM, cells thus affected were most abundantly localized to the normal extrusion zone at the borders of the crypt-surface epithelial cell units. DOC tended to cause a more generalized affection within the units than DDS. In spite of these deleterious effects, gaps corresponding to missing epithelial cells were not observed. TEM indicated the mechanism responsible for restoration of epithelial continuity in spite of extensive cell loss: The remaining epithelial cells seemed to flatten out and re-establish cell-to-cell contact by pseudopod formation along the basement lamina. This repair mechanism seemed to operate at a rapid rate; however, incomplete closure of cellular gaps i.e. small denuded parts of the basement lamina were occasionally observed. The results of this study are discussed in relation to a functional study under identical experimental conditions (Gastroenterol. Clin. Biol. 1981, 5, 124), in which these surfactants caused a significant alteration of normal colonic transport function.