Segments of gall bladder wall were then pinned out flat in a Petri dish under cooled oxygenated Krebs's solution.8 The serosa and tunica adventitia were removed to leave the tunica muscularis with attached mucosa. In 10 specimens the mucosal layer was removed by scraping with a scalpel blade. Several strips (usually four) 1Ox 2-3 mm in size were obtained from each gall bladder and the remaining tissue was used for histological study. It was found that at 20C, the gall bladder muscle deteriorated within a few hours, unlike muscle strips from other regions of the digestive tract.9 Experiments were therefore started within one hour of removal of the gall bladder. RECORDINGEach strip was suspended between parallel platinum electrodes in one of four identical 5 ml organ baths. The bathing fluid was Krebs's solution8 at 37°C and gassed with 95% oxygen and 5% carbon dioxide. Isometric tension was monitored with a strain gauge transducer. The tension was displayed on a pen recorder (Devices, Letchworth Garden City, Herts). Each preparation was subjected to a maximum initial tension of 0-1 g. STIMULATIONElectrical field stimulation was performed using rectangular pulses produced by a programmable digital stimulator. Tissues were stimulated at supramaximal voltage using 5-10 second trains 412 on 27 April 2019 by guest. Protected by copyright.

SUMMARYElectrical field stimulation of circular muscle strips from human lower oesophageal sphincter reveals a predominant relaxation response. This relaxation is non-adrenergic non-cholinergic (NANC). The nitric oxide synthesis-blocking agent Nw-nitro-L-arginine (10-100 uM) reduces or abolishes this NANC relaxation, suggesting involvement of nitric oxide in the response.

Strips from human gallbladder removed at surgery were exposed to cholecystokinin octopeptide CCK-OP 15 nM and were subjected to electrical field stimulation (EFS) in vitro using parameters for selective stimulation of nerves (5- to 10-sec trains of 0.3-msec pulses at 10 Hz). An adjacent strip from the same specimen was processed for histological examination. These preparations were given a numerical score for inflammatory change. The strength of contraction in response to CCK-OP was inversely related to the severity of inflammation. Gallbladders with no response to EFS had a higher inflammation score (median 11, range 5-16) than those with a response (median 7, range 3-12). We conclude that inflammatory changes in human gallbladder impair responses to neural and hormonal stimulation, but we are unable to determine unequivocally in this study whether this is a result of damage to nerves or muscle cells. However, the observation that some strips were able to contract in response to CCK-OP but not to neural stimulation suggests the possibility of neural damage in gallbladder inflammation.