1975
DOI: 10.1016/s0016-5085(19)32483-7
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Physiology of the Gallbladder

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Cited by 47 publications
(8 citation statements)
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“…The differences in the results of these earlier studies may possibly be explained on the basis of differences in methods (sonographic versus scintigraphic) and in patient populations with regard to the level, duration, and completeness of spinal cord injury 717-22 However, since cholecystokinin and vagal responses are preserved in patients with SCI and only the SNS to the gall bladder is impaired, our findings of normal gall bladder contractility and lower gall bladder fasting volume (suggestive of impaired gall bladder filling) in patients with SCI above T10 conform well to the established physiological facts about gall bladder contractility—that is, cholecystokinin and the vagus are important for gall bladder contraction,14 whereas the sympathetic nerve supply is mainly responsible for gall bladder relaxation during filling 1416 …”
Section: Discussionsupporting
confidence: 82%
“…The differences in the results of these earlier studies may possibly be explained on the basis of differences in methods (sonographic versus scintigraphic) and in patient populations with regard to the level, duration, and completeness of spinal cord injury 717-22 However, since cholecystokinin and vagal responses are preserved in patients with SCI and only the SNS to the gall bladder is impaired, our findings of normal gall bladder contractility and lower gall bladder fasting volume (suggestive of impaired gall bladder filling) in patients with SCI above T10 conform well to the established physiological facts about gall bladder contractility—that is, cholecystokinin and the vagus are important for gall bladder contraction,14 whereas the sympathetic nerve supply is mainly responsible for gall bladder relaxation during filling 1416 …”
Section: Discussionsupporting
confidence: 82%
“…The action of exogenous CCK is potentiated by electrical stimulation of the vagus (Pallin & Skoglund, 1964). Thus, it seems that the physiological control of the gall-bladder evacuation is by both neural and humoral mechanisms and that the orthodox view (Banfield, 1975) must be tempered. Periodic vagal release of gastrin is unlikely since interdigestive fluctuations in plasma gastrin have not been seen (Keane, Di Magno, Dozois & Go, 1980; and also because the gall-bladder is very insensitive to gastrin (Yau, Makhlouf, Edwards & Farrar, 1973).…”
Section: Discussionmentioning
confidence: 99%
“…The gall-bladder response to cholecystokinin (CCK) is not prevented by atropine, hexamethonium or vagotomy (Hong, Magee & Crewdson, 1956). These observations have led to the view that the gall-bladder is primarily controlled by a humoral mechanism (CCK) and that neural control is of minor importance (Banfield, 1975). This report is concerned with vagal control of the gall-bladder contraction which occurs in association with the periodic interdigestive activity of the upper gastrointestinal tract in fasting dogs (Boldyreff, 1911;Ivy, 1934;Itoh & Takahashi, 1981) and in response to acidification of the duodenal mucosa (Hong et al 1956).…”
Section: Introductionmentioning
confidence: 99%
“…The functions of the gall-bladder are absorption of water which leads to concentrate the hepatic bile and extrusion of cystic bile (Banfield, 1975). The process of extrusion of cystic bile is the co-operative performance of gall-bladder contraction and of relaxation of Oddi sphincter muscle, and it is regulated by chemical substances (Yau et al, 1973;Anderson et al, 1974;Yusko et al, 1983;Pomeranz et al, 1984), as well as by vagal innervation (Magee et al, 1984).…”
Section: Introductionmentioning
confidence: 99%