Sphincter of Oddi function in the Australian brush‐tailed possum is inhibited by intragastric ethanol

Abstract

The role of sphincter of Oddi (SO) function in alcoholic acute pancreatitis (AP) is unclear. We aimed to compare the effect of i.v. and intragastric (IG) ethanol on SO function (i.e. trans-sphincteric flow; TSF) and investigate possible neural mechanisms. The involvement of gastric mucosal damage was also investigated by pretreatment with pantoprazole. In anaesthetized Australian possums, blood pressure (BP), TSF and blood ethanol concentrations were measured after i.v. or IG ethanol. Possums were subjected to acute vagotomy, atropine, L-nitro arginine methyl ester (L-NAME) or pantoprazole pretreatment prior to IG ethanol. BP was not significantly altered by ethanol. Ethanol decreased TSF in a dose and route-dependent manner. The lowest dose of IG ethanol reduced TSF but this response was not duplicated by i.v. ethanol producing the same blood ethanol concentrations. Acute vagotomy, atropine or L-NAME pretreatment blocked the ethanol-induced decrease in TSF and simultaneously suppressed the blood ethanol concentration. Pantoprazole pretreatment reduced the TSF response and blood ethanol concentrations implicating mechanisms induced by gastric mucosal damage. We conclude that ethanol (and/or its metabolites) reduces TSF via humoral and neural mechanisms involving vagal pathways, muscarinic receptors and nitric oxide. Reduced TSF could contribute to the onset of AP.

Long-term outcomes in patients with gallstones detected by mass screening

“…Why drinkers are more likely to require cholecystectomy than other persons with gallstones is unknown. However, some studies demonstrated that ethanol decreased activity of the sphincter of Oddi . Such sphincteric dysfunction might increase risk of symptomatic gallstones.…”

Alcohol and the digestive system – should it always be blamed?

“…Obserwowane u osób przewlekle pijących alkohol spowolnienie motoryki jelitowej naraża je na nadmierny rozwój flory jelitowej, zwiększoną produkcję aldehydu octowego i translokację bakteryjną [72][73][74][75][76][77][78][79]. Nadmiar toksycznego aldehydu octowego wiąże się z białkami komórkowymi, co osłabia potencjał antyoksydacyjny, a tym samym odporność błony śluzowej.…”

Pancreatitis after percutaneous ethanol injection into HCC: a minireview of the literature

“…Furthermore, interesting animal studies have demonstrated that ethanol may have direct effects on the pancreas, such as microcirculatory changes and direct toxic damage to the pancreatic acini [ 22 - 24 ]. Moreover, the mechanism of ethanol-induced pancreatitis has been well-studied in an interesting animal model in which it was demonstrated that sphincter of Oddi dysfunction was implicated in several forms of acute and chronic pancreatitis [ 25 ]. In fact, according to the authors, since trans-sphincteric flow, regulated by the sphincter of Oddi which acts as a pump, is a direct measure of sphincter of Oddi function, an alteration of this trans-sphincteric flow after intragastric or i.v.…”

“…In fact, according to the authors, since trans-sphincteric flow, regulated by the sphincter of Oddi which acts as a pump, is a direct measure of sphincter of Oddi function, an alteration of this trans-sphincteric flow after intragastric or i.v. ethanol may indicate Oddi dysfunction; the authors also investigated whether neural mechanisms and gastric mucosal damage might play a role in this process [ 25 ], demonstrating that both intragastric and i.v. ethanol administration altered the Oddi trans-sphincteric flow.…”

“…They also suggested, in accordance with other studies [ 26 - 28 ], that the fall in Oddi trans-sphincteric flow might be due to the direct effects of ethanol, its metabolites (acetaldehyde) and/or other humoural agents (superoxide, endothelin-1) on sphincter of Oddi motility. Furthermore, an effect of ethanol and/or its metabolites on sphincter of Oddi nitrergic innervations was observed [ 25 ]. The authors thus concluded that reduced sphincter of Oddi function might contribute to elevated pancreatic duct pressure, which is one of the events required for the onset of acute pancreatitis [ 25 ].…”