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Gallbladder motility is controlled by a complex interplay of hormonal and neural factors. It is being recognized increasingly that the key mediators of gallbladder motility—the gastrointestinal peptides—act through both neural and hormonal pathways to influence gallbladder motility. Most significant gallbladder disease is associated with disturbances of normal motility. Experimental and clinical studies have demonstrated impaired motility in gallstone disease, and experimental evidence indicates that motility disturbances precede gallstone formation. Acute acalculous cholecystitis is seen frequently in patients with prolonged fasting and gallbladder stasis, and chronic acalculous cholecystitis actually is defined by demonstrable decreased gallbladder emptying.
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Tierney et al. (1993) studied this question.
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