Influence of Glucagon on Pancreatic Exocrine Secretion in Man

Dyck, Walter P.; Texter, E. Clinton; Lasater, John; Hightower, Nicholas C.

doi:10.1016/s0016-5085(70)80067-1

Cited by 133 publications

(31 citation statements)

References 23 publications

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“…For this purpose several hormones with inhibitory effects on the pancreas have been recommended, such as glucagon (Zajtchuk et al, 1967;Dyck et al, 1970), calcitonin (Schmidt et al, 1971), and SRIF , which all markedly depress the ecbolic and to a lesser extent the hydrokinetic pancreatic secretion. Knight et al (1971) first introduced glucagon in the treatment of acute pancreatitis and this was followed by several reports in favour of this new therapy.…”

Section: Discussionmentioning

confidence: 99%

Somatostatin therapy of acute experimental pancreatitis.

Lankisch¹,

Koop²,

Winckler³

et al. 1977

Gut

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SUMMARY Because somatostatin (SRIF) reduces exocrine pancreatic secretion, its effect on acute pancreatitis was investigated in rats. Linear SRIF reduced serum amylase and lipase but had no effect on pancreatic necrosis, oedema, leucocyte infiltration, and enzyme content. The mortality rate was not reduced. These results do not recommend the use of SRIF in the treatment of acute pancreatitis.Cyclic somatostatin (SRIF) significantly reduces hormonal Dollinger et al., 1976;Domschke et al., 1976) and non-hormonal stimulated pancreatic volume and enzyme secretion in man. Linear SRIF inhibits basal and hormonal stimulated enzyme secretion in the rat (Folsch et al., 1976). As 'rest to the gland' is generally considered to be a major aim in the treatment of acute pancreatitis (Trapnell, 1972) the effect of SRIF was investigated in acute experimental pancreatitis in the rat. MethodsAcute experimental pancreatitis was induced by retrograde injection of 0-6 ml of 0-8, 2-0, 2-5, and 3-0 Na-taurocholate (Serva Feinbiochemica, Heidelberg) into the pancreatic ducts of 101 male Wistar rats (180-220 g) (Lankisch et al., 1974). Linear SRIF (Serono, Freiburg) was given subcutaneously at a dosage of 200 ,ug during operation as a bolus injection followed by infusion of 100 ,ug/100 g body weight/h for three hours. This regime had been found to decrease significantly pancreatic enzyme secretion for more than four hours (Folsch et al., 1976). Controls received saline infusions. To investigate the SRIF influence upon the survival rate the following groups were formed (Figure) : (a) SRIFtherapy: n = 6; (b) controls: n = 5; 0-8 %-Na-taurocholate-pancreatitis was not used for survival experiments as the mortality rate of this model is too low to demonstrate the success of a treatment.To study the effects of SRIF upon morphological and enzymatic factors rats were killed four hours after induction of pancreatitis by 0-8, 2-0, and 3 0%-Na-taurocholate-that is, one hour after the treatment was stopped. 2 5%-Na-taurocholate-pancreatitis was not used as there were no distinct differences between 2-0 and 3 0 %-Na-taurocholate-pancreatitis where the above mentioned factors were concerned (Table). Ascites was measured and tissue from the head and the tail of the pancreas was fixed in Bouin's solution, embedded in paraffin, cut in 5 ,um sections, and stained with haematoxylin and eosin.

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Section: Discussionmentioning

confidence: 99%

Somatostatin therapy of acute experimental pancreatitis.

Lankisch¹,

Koop²,

Winckler³

et al. 1977

Gut

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“…The mechanisms responsible for these observations remain unclear, but pancreatic glucagon or a structurally related glucagon from the gut (enteroglucagon) are potential mediators (61). Supraphysiologic doses of glucagon inhibit pancreatic exocrine secretion in man, but no studies have compared plasma levels of glucagon after infusion of inhibitory doses and a meal.…”

Section: Glucagonmentioning

confidence: 99%

Neurohormonal Control of Human Pancreatic Exocrine Secretion

et al. 1995

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Near the end of the last century, Pavlov suggested that pancreatic secretion was exclusively controlled by neural reflex mechanisms (1). In 1902, Bayliss and Starling published their results on secretin, opening the field of gastrointestinal endocrinology while arguing that neural regulation of the pancreas is "superfluous and improbable" (2). In the following decades, especially after the discovery of cholecystokinin (CCK), it was generally held that exocrine pancreatic secretion is mainly regulated by hormones. Thus, investigators have historically tended to adopt an "all-or-nothing" approach; current appreciation of the complexity of mechanisms governing most biologic phenomena leads us to accept that the pancreas is regulated through an interplay of multiple neural and hormonal pathways.Several factors have impeded conclusive definition of the relative contribution of neural and hormonal control of pancreatic secretion. First, the information accumulated over the last several years clearly indicates that results obtained in one species cannot be directly transferred to another. Second, many conclusions were based on infusion of regulatory peptides at supraphysiologic concentrations, which may not accurately reveal their physiologic role. Sensitive and specific assays detecting postprandial plasma levels have now been established for most relevant substances. Third, even infusion of peptides at postprandial plasma levels may not fully elucidate their role as physiologic mediators.Plasma levels obtained from peripheral veins do not necessarily reflect concentrations at the pancreatic receptor, and exogenous infusion may not accurately mimic endogenous release. Fourth, selective receptor antagonists for the peptides in question have only recently become available. The application of effective receptor blockers (e.g., pentanoic acid and benzodiazepine derivatives for CCK receptors) has greatly aided our understanding of physiologic roles. Fifth, pancreatic function is regulated not only by peptide hormones from gastrointestinal endocrine cells, but also by regulatory peptides localized in pancreatic nerve fibers. Finally, pancreatic function is integrated through a complex interaction of mucosal, humoral, neural, and myogenic factors that regulate gastrointestinal secretion and motility. Analysis of a single factor allows only a limited view of pancreatic function as an integral component of the gastroenteropancreatic system.In this review, we have attempted to bring together findings from our groups and others, in order to provide an integrative concept of the neurohormonal systems controlling human exocrine pancreatic secretion. This overview evolved from the first Frank Pickering Brooks Basic Science Lecture, given by the first author at the American Pancreatic Association in 1992. For further review of the regulation of pancreatic exocrine secretion in man and other species, we also refer the reader to several excellent reviews published recently (3-7). EFFECTS OF EXOGENOUS ADMINISTRATION OF SECRETAGOGUESIntr...

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“…Dreiling and Janowitz [56], Lawrence [25], and Dyck et al [57] reported a decrease in gastric and pancreatic secretion after the administration of glucagon. A decrease in pancreatic secretions is highly desirable when examining the duodenum.…”

Section: Discussionmentioning

confidence: 99%

Gastrointestinal radiography with glucagon

Miller

Chernish

Brunelle

1979

Gastrointest Radiol

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This report summarizes the results of nine diagnostic radiographic studies done double blind crossover comparing glucagon to placebo and to anticholinergic drugs in volunteers. In seven studies the subjects were administered drug intramuscularly and in two studies intravenously. There were five diagnostic studies of the upper gastrointestinal tract, one for esophageal varices and three of the colon. The results indicate that glucagon can be given intramuscularly and intravenously. When given intravenously it has a rapid onset and predictable length of action depending on the dose given. Reports of side effects were few consisting primarily of nausea and or vomiting. These results indicate that glucagon is the drug of choice for hypotonic diagnostic examinations.

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Influence of Glucagon on Pancreatic Exocrine Secretion in Man

Cited by 133 publications

References 23 publications

Somatostatin therapy of acute experimental pancreatitis.

Somatostatin therapy of acute experimental pancreatitis.

Neurohormonal Control of Human Pancreatic Exocrine Secretion

Gastrointestinal radiography with glucagon

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