Whether K+ channel blockade can modify the effect of LPS induced hypo-contractility remains unknown. We therefore hypothesized that the blockage of K+ channel antagonizes LPS effect on mouse jejunal excitability and contractility. Methods: In organ bath, Vorinostat research buy mouse jejunum segments were perfused in oxygenated Kreb’s solution at 37°C.

The spontaneous slow wave activity and muscle strip contractility were respectively recorded by using suction electrode and isometric force transducer. After equilibrated for 45 min, slow waves were recorded in condition of control, in presence of LPS (30 ug/ml, 30 min) and in addition of TEA, 4AP, E-4031, Cisapride and LNNA, respectively. Results: 1. LPS treatment resulted in significant attenuation of slow wave activity.

Compared Selleck LY294002 to control, the LPS induced the baseline downshift indicating hyperpolarization. The normalized amplitude of slow wave was decreased to 0.38 ± 0.08 (n = 5, P < 0.05); the frequency (CPM) was decreased from 42 ± 6.5 to 21 ± 3.6 (n = 5, P < 0.01). 2. K+ channel blockade partially reversed the effect of LPS on slow wave activity. The baseline was elevated upshift by 4AP (1 mM), E-4031 (2 uM), Cisapride (1 uM) and LNNA (200 uM), in presence of LPS, indicating a reversible depolarization against to LPS. In addition, E4031 increased the frequency to 35 ± 3.3 (n = 5, P < 0.05) and prolonged the duration to 2.25 ± 0.5 sec from 1.66 ± 0.3 sec in control (n = 5, P < 0.05); the initiation of firing superimposed onto plateau was remarkable. 3. E-4031 attenuated the LPS induced hypo-contractility. The muscle strip contraction respectively from control, LPS and E4031 (2 uM, in presence of LPS) was 0.45 ± 0.03, 0.28 ± 0.04 and 0.33 ± 0.08 (g.mm-2.s-1; n = 3; ANOVA: P < 0.05). Conclusion: The results of acute LPS treatment in this study demonstrate that blockade ERG-K reverses LPS attenuations in excitability and contractility and a potential new insight into an independent pathway during LPS endotoxemia. Key Word(s): 1. Lipopolysaccharide; 2. Dysmotility; 3. ERG-K; Presenting Author: WANG YAN Additional Authors:

SHIHAI TAO, ZOUBAI CANG, JIANG JIONG, CHENFEN RONG, JIA MIAO Corresponding Author: WANG YAN Affiliations: Second Hospital of Medical College, Xi’an Jiaotong University Objective: Ghrelin medchemexpress is an orexigenic peptide with prokinetic effects. However, the mechanism and effects of ghrelin in regulating of the small intestinal motility are not fully understood. Our study aimed to explore the effects and mechanism of ghrelin on interdigestive myoelectric complex (IMC) in rats, as well as the neural pathway of it on the central nervous system (CNS) and the enteric nervous system (ENS). Methods: 1). Two pairs of silver bipolar electrodes were chronically implanted in the duodenum and jejunum of rats for electromyography. Ghrelin (20 μg kg-1) was injected intravenously into rats during fasting.