Hyperglucagonemia, hypocalcemia and diminished gastric blood flow-evidence for an etiological role in stress ulcer of rat

Schwille, P. O.; Schellerer, W; Reitzenstein, M.; Hermanek, P.

doi:10.1007/bf01924210

Cited by 11 publications

(9 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During stress conditions we repeatedly confirmed the existence of basal hyperglucagonemia [24,26] and a reduction of MBF and acid [10,11,15,24,33]. The latter is determined predominantly by the reduced secretory volume, the reduced acidity of the gastric juice making only a minor contribution.…”

Section: Gastric Parameterssupporting

confidence: 68%

“…At present, the stress-mediated decrease in mucosal blood flow (MBF) is con- sidered a critical variable [14]. In immobilization stress of the rat, a common neurally mediated kind of stress for induction of ulcers, MBF, and also acid secretion are decreased [10,11,15,24,33], while A-cell glucagon in plasma is elevated [24,25,26]. In a number of species, exogenous glucagon inhibits acid secretion [9].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Influence of exogenous glucagon on gastric acid secretion, mucosal blood flow, and stress ulcers in the rat: Dose-response results under non-stress conditions and immobilization stress

et al. 1983

Self Cite

View full text Add to dashboard Cite

In non-stressed rats and rats stressed by immobilization, gastric secretion (acid, pepsin), mucosal blood flow (MBF), stress ulcers as well as glucose, insulin, and glucagon in blood were studied during 8 h, with and without additional infusion of exogenous glucagon (0.2, 1.4, 9.8 micrograms/kg/h). Metabolic clearance of glucagon and the disappearance half-time of exogenous glucagon from blood do not differ during zero stress and stress, a fact that favors the assumption of hypersecretion of glucagon as the cause of stress hyperglucagonemia. During stress alone acid secretion (volume, acidity) and MBF are lower than during zero stress; pepsin remains unchanged. Under zero stress condition additionally administered glucagon inhibits pepsin and MBF, but not acid secretion, in a dose-dependent manner. The ulcer index increased without changing the severity of ulcers. During stress the intermediate and highest glucagon doses stimulate MBF and pepsin secretion, other variables remaining unchanged. It is concluded that glucagon effects on functions of the gastric mucosa in the rat vary fundamentally, depending upon the environmental conditions.

show abstract

Section: Gastric Parameterssupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Influence of exogenous glucagon on gastric acid secretion, mucosal blood flow, and stress ulcers in the rat: Dose-response results under non-stress conditions and immobilization stress

et al. 1983

Self Cite

View full text Add to dashboard Cite

show abstract

“…Our previous findings (12,13) of hyperglucagonemia, hypocalcemia and diminished gastric blood flow during restraint stress led us to assume that stress itself may be followed by a hitherto unknown sequence of hormonal events altered CT release included. Therefore we investigated whether CT plays a role during stress hypocalcemia in various rat models with or without endogenous CT sources.…”

Section: Glucagon -Gastrin -Serum Calcium -Ulcer Indexmentioning

confidence: 97%

Role of calcitonin in stress ulcer formation of various rat models. Preliminary report

et al. 1975

Self Cite

View full text Add to dashboard Cite

S~y:During restraint stress (24 h) various rat models exhibit differences in ulcer index, a decrease in gastric perfusion (P02) , serum gastrin and calcium, but increased pancreatic glucagon. Prophylaxis by calcitonin prevents gastrin from falling, improves markedly ulcer index in intact, sham-operated and thyroparathyroidectomized rats, is ineffective following parathyr0idectomy and augments stress sensivity following thyroidectomy. It is suggested that, in the presence of exogenous calcitonin, both vulnerability of gastric mucosa and responsiveness of pancreatic alpha cells largely depend on concentration of extracellular calcium and availability of endogenous thyroidal calcitonin and parathyroid hormone.Key words: rat models -stress ulcers -calcitonin prophylaxis -mucosal pO 2 -glucagon -gastrin -serum calcium -ulcer index Exogenous calcitonin (CT) is said to diminish gastric secretion in humans (4, II, 15) and animals (5, 9, 15) and to prevent stress induced gastroduodenal ulceration in rats (2, 8). Our previous findings (12, 13) of hyperglucagonemia, hypocalcemia and diminished gastric blood flow during restraint stress led us to assume that stress itself may be followed by a hitherto unknown sequence of hormonal events altered CT release included. Therefore we investigated whether CT plays a role during stress hypocalcemia in various rat models with or without endogenous CT sources. Furthermore, the response to exogenous CT of those exactly defined defect animals was evaluated with special emphasis to serum gastrin. ANIMALS AND METHODSRandomized male Sprague-Dawley rats (SPF, 180 -200 g b.w.), fed normal laboratory chow (C IOOO, Altromin, Lage) were divided in 30 animals per group and left either intact or were prepared microsurgucally (pentobarbital-Na anesthesia) as following: intact; sham operated (sham); parathyroidectomized (PX); thyroidectomized (TX) and thyroparathyroidectomized (TPX) with oral replacement of thyroxine ( + T4; 600 ~g/l deionized drinking water). After 1 week each group was subdivided (n = 8 -I0) one third servind as controls. The remaining two thirds were either exposed to stress alone or received repeated

show abstract

“…Besides its gluconeogenetic effects, this hormone, when administered exogenously, is discussed to be involved in the regulation of renal sodium excretion [3,4,14]. In a recent report it was suggested that stress-induced glucagonemia might play a role in the pathogenesis of acute gastric ulcerations [15] by way of its possible interference with gastric blood perfusion or gastric mucosal microcirculation [19]. The aim of the present study was to search for changes of hemodynamics in the presence of elevated endogenous pancreatic 1 glucagon (pG1) 2 in the dog.…”

mentioning

confidence: 99%

Hemodynamic splanchnic and renal changes associated with administration of arginine-hydrochloride in dogs

et al. 1980

Self Cite

View full text Add to dashboard Cite

Summary.The relationship of arginine-mediated release of endogenous glucagon and insulin to renal and splanchnic arterial blood flow, blood pressure, and heart rate was studied in dogs. Intravenous injection of argininehydrochloride (arg-HC1) in logarithmically increasing doses increased the concentration of glucagon (pG1) in the femoral artery from 143 + 39 pg/ml (pre-injection) to 282 +49 pg/ml (following maximum dosage of arg-HC1) and insulin concentration from 23 +5 to 41 + 11 gU/ml. Sodium chloride (NaC1) and urea, isovolemic and isosmolar to arg-HC1, failed to change pG1 and insulin. Arg-HC1 depressed arterial blood pressure from 93 + 13 (preinjection) to 60 + 14 mm Hg (maximum dose), NaCI increased it from 89 _+ 13 to 99 _+ 13 m m H g . The blood flow increase due to arg-HC1 was comparable with that due to NaC1 in renal as well as in celiac and left gastric artery. The former was more pronounced in superior and inferior pancreaticoduodenal artery by 61 and 102%, and in gastroduodenal and superior mesenteric artery by 11 and 35%. Infusion of arg-HC1 increased pG1 from 294+90 to 731 _+ 200 pg/ml, and insulin from 23 + 5 to 63 +_ 18 ~tU/ml; the resulting blood flow increase, however, only differed in both pancreatic arteries by 10-20% from the rise during Nac1 infusion where no change ofpG1 was observed and a decline occurred in insulin from 64+ 21 to 27 + 8 pU/ml. It is concluded that physiological levels of pG1 have no systemic effect on arterial blood flow. A local flow increasing effect of glucagon and/or insulin on the arteries next to the pancreas is discussed.Key words: Arginine-hydrochloride -Endogenous glucagon -InsulinArterial blood flow -Arterial blood pressure -Heart rate Despite great progress made in physiology and pathophysiology of gastrointestinal hormones, little is known about hemodynamic effects of those peptides. From the available literature it is apparent that most work conducted so far deals

show abstract

Hyperglucagonemia, hypocalcemia and diminished gastric blood flow-evidence for an etiological role in stress ulcer of rat

Cited by 11 publications

References 10 publications

Influence of exogenous glucagon on gastric acid secretion, mucosal blood flow, and stress ulcers in the rat: Dose-response results under non-stress conditions and immobilization stress

Influence of exogenous glucagon on gastric acid secretion, mucosal blood flow, and stress ulcers in the rat: Dose-response results under non-stress conditions and immobilization stress

Role of calcitonin in stress ulcer formation of various rat models. Preliminary report

Hemodynamic splanchnic and renal changes associated with administration of arginine-hydrochloride in dogs

Contact Info

Product

Resources

About