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PubMed2005

Class I antiarrhythmics inhibit Na+ absorption and Cl- secretion in rabbit descending colon epithelium.

To clarify the mechanism of the diarrhea associated with the clinical use of antiarrhythmic drugs we assessed the effects of these agents on transepithelial Na+ absorption and Cl- secretion, on basolateral K+ conductance, and on the properties of single basolateral K+ channels of rabbit colon epithelium. Quinidine and propafenone, both at 10 microM, inhibited Na+ absorption by 27 and 38% respectively, compared with 50% with 5 mM Ba2+. The other tested class I antiarrhythmics disopyramide, mexiletine, lidocaine, and flecainide decreased Na+ current by 9-13%. Procainamide and the class III antiarrhythmics N-acetylprocainamide, sotalol, ibutilide, and amiodarone were no or were very weak inhibitors of Na+ absorption. Cl- secretion, stimulated with the adenosine analogue NECA (5'-N-ethylcarboxamide-adenosine), was reduced by 54% with quinidine and by 29% with propafenone compared with 100% with Ba2+. Mexiletine, lidocaine, and flecainide inhibited Cl- secretion by 10-23%, whereas the class III antiarrhythmics were no or were weak inhibitors. Those antiarrhythmics that inhibited Na+ and Cl- transport also reduced basolateral K+ conductance, determined in amphotericin B permeabilized epithelia. The activity of the high-conductance, Ca2+-activated, voltage-dependent K+ (BK(Ca)) channel, which is primarily responsible for basolateral K+ recycling during Na+ absorption, was inhibited by 10-30 microM quinidine or propafenone in the form of a rapidly dissociating block. Mexiletine and flecainide inhibited the single channel conductance at higher concentrations; disopyramide, lidocaine, and procainamide were ineffective. In conclusion, the present evidence suggests that the diarrhea caused by class I antiarrhythmic drugs such as quinidine and propafenone is a result of a reduction in basolateral K+ conductance and inhibition of BK(Ca) channels, thereby impeding transepithelial Na+ and water absorption.

Animals↗
PubMed2002

Prospective, randomized trial comparing sigmoid vs. descending colonic J-pouch after total rectal excision.

PURPOSE: The aim of this study was to compare the bowel function of sigmoid vs. descending colonic J-pouches after ultralow anterior resection for rectal cancer. METHODS: A prospective, randomized trial was conducted from March 1998 to September 1999. Ninety-two consecutive patients undergoing ultralow anterior resection for cancers arising from 3 to 10 cm from the anal verge were recruited. Forty-eight patients were males; the mean ages (standard error of the mean) for patients with sigmoid and descending colon pouches, respectively, were 65.2 (3.1) years and 62.3 (3.1) years. A total of 46 patients were randomly assigned to each group. Two patients from each group were excluded; abdominoperineal resection was performed for two patients in the sigmoid pouch group and one patient in the descending pouch group. One patient in the descending pouch group had a transanal resection of a benign polyp. Dukes staging and use of postoperative chemoradiotherapy were statistically similar in both groups. All patients underwent a standardized ultralow anterior resection. A defunctioning loop ileostomy was used routinely. Anorectal physiology and bowel function questionnaires were performed at six weeks after ileostomy closure and again at 6 and 12 months after surgery. RESULTS: Median follow-up was 12 (range, 7 to 25) and 12 (range, 6 to 25) months, respectively, for sigmoid and descending pouch groups. Median tumor and anastomotic heights, time to ileostomy closure, operative time, and postoperative stay were statistically similar in both groups. There were no significant differences in stool frequency, incontinence, urgency, use of pads and antidiarrheals, sensation of incomplete evacuation, and anorectal physiology results between groups (P > 0.05). CONCLUSION: Pouches made from sigmoid or descending colon give similar bowel function after ultralow anterior resection for rectal cancers.

Adenocarcinoma↗
PubMed1982

Active potassium transport by rabbit descending colon epithelium.

Previous studies of rabbit descending colon have disagreed concerning potassium transport across this epithelium. Some authors reported active K+ secretion under in vitro short-circuited conditions, while others suggested that K+ transport occurs by passive diffusion through a highly potassium-selective paracellular route. For this reason, we re-examined potassium fluxes across the colon in the presence of specific and general metabolic inhibitors. In addition, electrochemical driving forces for potassium across the apical and basolateral membranes were measured using conventional and ion-sensitive microelectrodes. Under normal conditions a significant net K+ secretion was observed (JK net = -0.39 +/- 0.081 mueq/cm2hr) with 42K fluxes, usually reaching steady-state within approximately 50 min following isotope addition. In colons treated with serosal addition of 10(-4)M ouabain, JKsm was lowered by nearly 70% and JKms was elevated by approximately 50%. Thus a small but significant net absorption was present (JKnet = 0.12 +/- 0.027 mueq/cm2hr). Under control conditions, the net cellular electrochemical driving force for K+ was 17mV, favoring K+ exit from the cell. Cell potential measurements indicated that potassium remained above equilibrium after ouabain, assuming that passive membrane permeabilities are not altered by this drug. Net K+ fluxes were abolished by low temperature. The results indicate that potassium transport by the colon may occur via transcellular mechanisms and is not solely restricted to a paracellular pathway. These findings are consistent with our previous electrical results which indicated a nonselective paracellular pathway. Thus potassium transport across the colon can be modeled as a paracellular shunt pathway in parallel with pump-leak systems on the apical and basolateral membranes.

Animals↗