Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Controversy exists in the literature concerning the effects of insulin and glucagon on cardiac muscle contractility, in particular during anoxia, ischemia or sepsis. The purpose of the present study was to determine the effects of insulin and glucagon on the systolic function of the normal and the dysfunctioning septic rat myocardium in the Langendorff preparation. In the normal isolated rat heart, neither insulin nor glucagon exhibited any lasting inotropic effect on systolic function or coronary flow. Sepsis (cecal ligation and puncture) resulted in a dramatic reduction of systolic function to 44% of control animals. All insulin-containing formulations tested improved systolic function in septic hearts by a mean of 85% compared to Krebs and glucose only. However, this improvement did not reach statistical significance compared to the use of Krebs and glucose only. Glucagon at 100 micrograms/l was doing as well as Krebs and glucose alone while at 1 mg/l glucagon was only able to maintain pre-perfusion contractility. Our results suggest that neither insulin nor glucagon seem to possess special inotropic properties for the isolated perfused normal or septic rat heart.
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PMID:The effect of insulin and glucagon on systolic properties of the normal and septic isolated rat heart. 390 99

Microcirculatory derangements in the pancreas associated with acute pancreatitis may contribute to a low-flow state and lead to pancreatic necrosis. This study investigated the effects of glucagon, a selective mesenteric arterial dilator, on pancreatic ischemia in canine bile-trypsin-induced pancreatitis (BTP). Measurements of cardiac Index (CI), total pancreatic blood flow (QP), pancreatic oxygen consumption (O2CP), and pancreatic arteriovenous shunt flow (QAVS) were obtained prior to and after inducing BTP. Bile-trypsin-induced pancreatitis was induced in 18 dogs. Nine received lactated Ringer's solution alone (LRPAN) at 6.5 mL/kg/hr, nine received lactated Ringer's solution plus continuous Intravenous (IV) glucagon hydrochloride (GLUPAN) at 1.0 micrograms/kg/min, and nine undergoing periportal dissection without BTP received IV glucagon (GLUCON). Following BTP, CI, QP, and O2CP decreased significantly and QAVS remained unchanged in crystalloid-treated animals (LRPAN). Glucagon administration (GLUPAN) transiently increased CI and QP but failed to improve O2CP and did not change QAVS. The decrease in O2CP observed after BTP in association with a constant QAVS suggests a metabolic block to oxygen uptake at the cellular level. Glucagon in pharmacologic doses does not reverse abnormalities in O2CP and is therefore of questionable physiologic benefit in the treatment of acute pancreatitis.
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PMID:Efficacy of pharmacologic glucagon in acute experimental pancreatitis. 397 Jun 71

The purpose of this study was to determine the optimal timing of intravenous glucagon infusion for the treatment of acute occlusive mesenteric ischemia. The superior mesenteric artery (SMA) was occluded for 85 min in 106 Sprague-Dawley anesthetized rats. The animals were divided into 12 treatment groups according to the timing of glucagon and saline administration, and survival was measured to 48 hr. Without treatment, all rats died within 24 hr. Intravenous saline (10 ml/kg/hr) for 2 hr did not significantly improve 48-hr survival (17-33%). Glucagon (1.6 micrograms/kg/min iv) plus saline (10 mg/kg/hr iv) for 2 hr after SMA occlusion significantly improved survival from 33% (saline control) to 83% (P less than 0.02). The same treatment begun 1 hr before SMA release (during ischemia) did not significantly improve survival (33% at 48 hr). Glucagon infusion during occlusive mesenteric ischemia was detrimental when added to effective postischemia treatment, reducing survival from 83 to 33% (P less than 0.02). Adequate saline infusion was required for glucagon efficacy after ischemia, as shown by an intermediate 48-hr survival of 50% when only maintenance saline (1.5 ml/kg/hr) was given. These data suggest that glucagon therapy should be delayed until after operative release of an acute SMA occlusion and should be accompanied by vigorous volume expansion.
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PMID:Effect of intravenous glucagon on the survival of rats after acute occlusive mesenteric ischemia. 399 Feb 72

The aim of this paper is to elucidate the cause of death after 90 min of normothermic partial (2/3) ischemia of the liver and to examine the effects of glucagon, somatostatin, insulin, prednisolone and oral administration of polymyxin B (PB). The animals 24 hr after partial ischemia for 90 min were divided into two groups; namely, animals with normal appearance and those with moribund state. There were no significant differences in the plasma level of S-GOT, S-GPT, amino acids, NH3 or insulin, or in morphometrically estimated volume ratio of necrotic hepatocytes between the two groups of rats. The blood glucose level, however, was significantly decreased (31 +/- 28 mg/100 ml, n = 6) in the moribund rats with a higher incidence of positive Limulus gelation tests as compared with the rats with normal appearance (149 +/- 19, n = 5). The 1-day and 1-week survival rates of the animals were 42/62 (69%) and 32/61 (53%), respectively. A glucagon injection (1.5 mg/kg, after ischemia) was effective to elevate the 1-day survival rate (14/14), but failed to increase the 1-week survival rate (11/14). On the other hand, a somatostatin injection (100 micrograms/kg, after ischemia) or PB treatment (15 mg/kg/day x 5-9, before ischemia) succeeded to increase the 1-week survival rate (20/22 p less than 0.01 and 17/17 p less than 0.01, respectively), although no significant amelioration in transaminase levels or volume ratio of necrosis was demonstrated. It could be seen that a moribund state after partial ischemia was accompanied by severe hypoglycemic shock, and that the injection of somatostatin after ischemia or the annihilation of gram-negative bacteria by means of oral administration of polymyxin B before ischemia prevented the occurrence of the hypoglycemic shock.
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PMID:Postischemic liver damage in rats: effect of some therapeutic interventions on survival rate. 629 17

The pancreases of 17 patients who had cystic fibrosis with and without diabetes mellitus were evaluated at autopsy by routine staining and immunohistochemical methods for insulin, glucagon, somatostatin, and pancreatic polypeptide. Qualitative assessment of the number of islets of Langerhans and the degrees of exocrine pancreatic atrophy, fibrosis, and fat replacement was made for each pancreas. Quantitative assessment of islet composition was performed in 15 of the 17 based on the immunochemical reactivity of each cell type. Nondiabetic patients with cystic fibrosis in the latter part of the first decade of life have classic fibrocystic changes of the pancreas, with some persisting exocrine tissue, islets that appear normal, and prominent nesidioblastosis. The latter process may protect these patients from glucose intolerance. Young adult diabetic patients with cystic fibrosis have total loss of exocrine pancreas with fat replacement, lack of nesidioblastosis, a qualitative decrease in the number of islets, fibrosis of and amyloid deposits in islets, decreased numbers of insulin-containing cells in each islet, and atrophy of islet cells, probably resulting from progressive ischemia. Although the potential exists for an increasing incidence of diabetes mellitus in patients with cystic fibrosis as their life spans increase, individual variation occurs in this disease.
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PMID:Endocrine pancreas in cystic fibrosis: an immunohistochemical study. 636 38

Effects of glucagon and prostacyclin (PGI2) were studied in anesthetized dogs during sequential occlusive and postocclusive mesenteric ischemia induced by 90 min of tourniquet stenosis of the superior mesenteric artery (SMA). After 30 min of SMA stenosis, glucagon (1 microgram/kg/min, n = 7), PGI2 (30 ng/kg/min, n = 7), or saline (1 ml/min, n = 3) was infused intravenously for 30 min, followed by 30 min of continued ischemia. SMA flow and distal SMA pressure ( SMAP ) decreased 76% with SMA stenosis (P less than 0.01). Ileal wall flow measured by radiolabeled microspheres decreased from 45 to 13 ml/min/100 g (P less than 0.01); mesenteric AV O2 difference ( AVDO2 ) increased from 5.1 to 10.1 ml/dl (P less than 0.01); and mesenteric O2 consumption (VO2) decreased by 48% (P less than 0.05). Glucagon infusion caused a further decrease in ileal wall flow, to 10 ml/min/100 g (P less than 0.05), and an increase in AVDO2 to 11 ml/dl (P less than 0.05), despite a 22% increase in cardiac output. PGI2 caused a similar decrease in ileal wall flow and an increase in AVDO2 , although these were not statistically significant. Saline infusion caused no change in measured variables. In the second phase of this study, SMA blood flow was restored by tourniquet release. After animals had stabilized for 30 min, a repeat 30-min drug infusion was studied. In this postocclusive period, persistent gut ischemia was indicated by a reduction in VO2 to 76% of original baseline, associated with a 50% decrease in both CO and SMAQ . Intravenous infusion of glucagon at this time increased SMAQ by 195% (P less than 0.05) and resulted in a return of VO2 to its original baseline level. PGI2 infusion caused a 21% increase in SMAQ and a 16% decrease in AVDO2 (NS), but had no significant effect on VO2. Glucagon was effective in the management of postocclusive mesenteric ischemia but appeared to have a detrimental effect on ileal blood flow in severe occlusive ischemia.
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PMID:Effects of glucagon and prostacyclin in acute occlusive and postocclusive canine mesenteric ischemia. 637 91

An experimental model of acute mesenteric ischemia following 85 minutes of superior mesenteric artery (SMA) occlusion in male Wistar rats was used in this investigation. Untreated control animals had a 48-hour survival rate of 38% (n = 26), whereas sham laparotomy resulted in a 100% 48-hour survival rate (n = 10). Study groups received intravenous infusions of normal saline solution (16.6 ml/kg/hr; n = 26) or similar volumes of normal saline solution with the addition of glucagon (1.6 micrograms/kg/min; n = 26), dopamine (3.2 micrograms/kg/min; n = 26), or prostacyclin (PGI2) (10.7 ng/kg/min; n = 26). Infusions were begun 15 minutes after initiating 85 minutes of SMA occlusion and were continued for a total of 90 minutes. Glucagon increased the 48-hour survival rate to 85%, significantly greater than both control survival (p less than 0.001) and normal saline solution group survival rates (p less than 0.025). Neither normal saline solution alone nor dopamine significantly increased the 48-hour survival rate, which was 54% in both groups. The PGI2 group survival rate, 65% at 48 hours, was significantly greater than the control rate (p less than 0.05), was not statistically different from the normal saline solution group survival rate, and was 20% less than the glucagon group survival rate, the latter difference approaching statistical significance (p = 0.10). Methylprednisolone (40 mg/kg; n = 26) administered as an intravenous bolus 15 minutes after initiating SMA occlusion significantly increased the 48-hour survival rate to 73% (p less than 0.01), whereas neither intravenous heparin (150 U/kg; n = 26) nor superoxide dismutase (11,900 U/kg; n = 26) were beneficial. Glucagon, methylprednisolone, and PGI2 improved the survival rate in this model of acute mesenteric ischemia.
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PMID:Pharmacologic interventions in acute mesenteric ischemia: improved survival with intravenous glucagon, methylprednisolone, and prostacyclin. 638 66

Plasma levels and renal uptake of gastrin were determined in ten dogs submitted to complete liver devascularization in order to induce an acute liver failure. Renal function was evaluated by renal plasma flow (RPF) and glomerular filtration rate (GFR) determinations. Liver devascularization was obtained by end-to-side porto-caval shunt (PCS) followed by temporary clamping of the hepatic artery. PCS alone did not affect renal function and renal ability to remove gastrin; after hepatic ischemia, both RPF, GFR and renal extraction of gastrin showed an abrupt decrease. At the end of the period of hepatic ischemia 5 dogs were submitted to glucose infusion, in consideration that: i) glucagon is able both to affect gastrin release and renal hemodynamics, and ii) hypoglycemia that develops after liver failure releases elevated amounts of glucagon. The renal handling of gastrin was not related to glucagon plasma levels, though the higher gastrin levels occurred at the lower glucagon concentrations. These data suggest that in acute liver failure there is a striking decrease of the renal clearance of gastrin associated with the impairment of kidney function. Furthermore, in this pathological condition plasma gastrin levels are affected by blood glucose concentrations through its effect on plasma glucagon levels.
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PMID:Plasma levels and renal removal of gastrin after acute hepatic ischemia in dogs. 647 Apr 35

In 31 dogs chronically beta blocked with oral propranolol (12 to 14 mg/kg/day), glucagon (20 micrograms/kg) and combined dopamine (10 micrograms/kg/min) and isoproterenol (0.2 micrograms/kg/min) were given intravenously and tested for hemodynamic efficacy. Dogs were divided into four groups. Basal hemodynamics were obtained In Group I (n = 8) without cardiopulmonary bypass. In Group II (n = 8), hemodynamics were studied after 15 minutes of global ischemia during cardiopulmonary bypass. In Group III (n = 8), hemodynamics were studied after regional ischemia produced by ligation of the proximal left anterior descending coronary artery. In Group IV (n = 7), myocardial oxygen consumption and left ventricular mechanics were studied before and after 1 hour of cardiopulmonary bypass. Our results indicate the following: (1) Dopamine-isoproterenol improves hemodynamics in basal, post-global ischemic, and post-regional ischemic states. Glucagon improves hemodynamics either insignificantly or to a lesser extent than dopamine-isoproterenol. Furthermore, glucagon produces a larger increase in heart rate, which is not desirable. (2) Both dopamine-isoproterenol and glucagon increase myocardial oxygen consumption in comparison with control.
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PMID:Pharmacologic antagonism of propranolol in dogs. III. Effects of dopamine-isoproterenol and glucagon on hemodynamics and myocardial oxygen consumption in ischemic hearts during chronic propranolol administration. 671 51

Segmental pancreatic autotransplantation is successful in our hands if blood flow through the splenic artery is enhanced by either a jump graft or a distal fistula, and if these technical manoeuvres are supplemented by anticoagulation. We found the jump method of arterial anastomosis was the most successful. Perfusion of the isolated graft is not necessary, and may even be harmful. Ischemia up to 3 hours appears to be well tolerated. The intraperitoneal location of the graft does not affect outcome, but preservation of the left gastric artery reduces mortality secondary to stomach and omentum ischaemia. Animals must be supplemented with Viokase 10 tablets daily. If the remaining pancreas has been removed graft function is best assessed by monitoring blood sugars. No animal recovers which becomes diabetic under these conditions. Serum insulin, serum glucagon and glucose tolerance tests (with or without calculation of K values) are no more useful than blood glucose to recognize graft loss.
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PMID:Pancreatic autotransplantation. 676 31


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