In the model of acute pancreatitis, under pentobarbital anesthesia (50 mg/kg body weight), a laparotomy was performed and 5% sodium taurocholate (1 ml/kg body weight) was injected into the biliopancreatic duct of the rat in one minute. Then the rat recovered from the anesthesia and was allowed access to water. Paxilline (2.2 μg/kg) was intravenously injected to rats 1 h before or after the injection of sodium taurocholate, respectively. Treatment with paxilline inhibited lockade inhibited the release of inflammatory mediators in rats during acute pancreatitis.

To study inhibition of BK channels, HEK293 cells were transfected with human BK channel alpha-subunit. Whole-cell patch clamp technique was used to study effect of paxilline. The initial membrane potential was 23 mV and characterized by brief hyperpolarizing fluctuations caused by spontaneous channel openings. Application of 1uM paxilline depoarized the cell to -5mV and completely blocked the BK current. The effect of th~ BK-channel blocker paxilline on activation curves was studied in the presence of 0.5 and 30 uM Ca2+. At 30 uM internal Ca2+the maximal current amplitudes in the presence of 30 and 100 nM mixilline were decreased relative to the control experiment. The IC50 value of paxilline was estimated at 50 nM.