physiology of the biliary tree motility of the gallbl bladder-part 1

An incomplete picture has emerged of the complex means by which gallbladder motility is controlled under normal and pathophysiological conditions. In the first part of this review an overall account is presented. The mechanisms of cholecystokinin release, its stimulation by dietary factors and peptides elaborated by both pancreas and small intestine are discussed. The inhibition of cholecystokinin release by bile acids and proteases is also described. In the second part attention is focussed on other peptides affecting motility. These include [a] octreotide, effective for treatment of acromegaly, [b] peptide YY, contributing to a "colonic brake", [c] motilin, associated with interdigestive contractions, analogues of which possibly correct gallbaldder hypomotility, and d] substance P and calcitonin gene- related peptide, which facilitate ganglionic transmission after release from exrinsic sensory neurones and alter gallbladder responses to vagal stimulation. The sympathetic nervous system and diabetes mellitus also influence vagal responses. The former, acting presynaptically, may provide a "brake" to prevent vagal overactivity. The latter could cause hypomotility via autonomic neuropathy, although hyperglycaemia, itself, may play a role. The role of nitric oxide, released from neurones also producing vasoactive intestinal peptide is recognized. Both lengthen muscle, the former producing responses without requiring plasma membrane receptors. Gallbaldder motility also changes during pregnancy and stone formation. Progesterone and cholesterol can limit G protein actions, thus impairing contractions. Inflammation is associated with abnormal motility. The production of reactive Oxygen metabolites, acting directly or releasing prokinetic prostaglandins, may be responsible. It has been proposed that the gastrointestinal tract may be normally in a state of controlled inflamation, primed to react to harmful challenges

Swallowing-induced cardio-respiratory responses in man

Swallowing transiently increases heart rate. One of the authors developed pronounced bradycardia while breath holding, particularly after an expiration. The objective, therefore, was to study his cardiac responses during swallowing as pronounced bradycardia developed. When, after a maximum inspiration [supine], the heart rate slowly fell below 50 beats min-1 well-defined P waves [lead II] disappeared. By swallowing 6 times on command after the P waves disappeared his heart rate increased immediately [68 +/- I beats min-1 n=6]. P waves with similar morphology to those pro-swallowing were recorded 0.7 +/- 0.1 s [n=6] after the first swallow. He continued breath holding after swallowing. P waves again disappeared although at faster heart rates [57 +/- I beats min-1; n=6]. Furthermore, well-defined P waves were observed after the second disappearance at heart rates within the range 30-40 beats min-1 Small amplitude P waves continued to be recorded from lead I with P wave disappearance in lead II, suggesting a pacemaker shift although not to the av node. Autonomic nerves can shift the dominant pacemaker within the sa node. The present report indicates that increased vagal tone may be rapidly reversed by swallowing