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)

The work demonstrates the efficacy of glucagon in acute myocardial infarction and its complications, particularly in bradycardia, hypotension, disorders of cardiac rhythm and conduction, cardiogenic shock, cardiac insufficiency in complete atrioventricular heart block and recurrent forms of ventricular fibrillation. A differential approach and dynamic control over the effect of the drug on the values of hemodynamics, respiration, and metabolism are necessary under the conditions of units of intensive therapy and cardioresuscitation.
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PMID:[Differential use of glucagon in acute period of myocardial infarct]. 31 54

Carbohydrate metabolism is temporarily disturbed in acute myocardial infarction. The degree of hyperglycaemia and failure of response of insulin appears to be related to the severity of the infarction. The underlying hormonal changes probably include increased secretion of catecholamines and of glucagon. Circulating free fatty acids (FFA) are generally increased by the same metabolic and hormonal factors which promote glucose intolerance. In the zone of developing infarction in the heart, there is a complex metabolic situation with glucose metabolism both being accelerated and inhibited by different factors. Continued uptake of FFA is associated with intracellular accumulation of activated long-chain FFA, acyl CoA, which tends to inhibit mitochondrial metabolism. The metabolism of glucose is thought to be beneficial and that of FFA detrimental to the infarcting tissue. Thus the glucose intolerance and the high circulating FFA occurring as part of the general metabolic response to myocardial infarction, are thought to be harmful to the ischaemic tissue. Increased provision of glucose by dichloroacetate, and inhibition of FFA metabolism by nicotinic acid analogues decrease the extent of experimental infaraction, while glucose--insulin--potassium and propranolol act both by increasing glucose uptake and decreasing that of FFA. Glucose intolerance is also common in peripheral vascular disease. The reasons for this are obscure. However, the alterations in circulating insulin concentration which accompany this intolerance may be involved in the development of arterial lesions either directly through an effect on arterial wall synthesis or indirectly through an effect on circulating lipid levels. Defects may also be found in arterial wall mucopolysaccharide or sorbitol metabolism. The role of sex hormones and catecholamines remains speculative. At present the most cogent view is that in peripheral vascular disease a multi-hormonal disorder exists which may be contributing to the development of arteriosclerosis.
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PMID:Carbohydrate metabolism in cardiovascular disease. 79 85

Data on 80 cases of myocardial infarction complicated by different forms of ventricular fibrillation (VF)--primary, secondary and recurrent--are analysed. VF was shown to be accompanied by distinct disorders in respiration, metabolism and haemodynamics. Metabolic disorders are characterized by acid-base and electrolyte balance changes, increased activity of the adrenal glands, and increased release of catecholamines and glucocorticoids into the blood. The latter proves that VF increases the stress reaction of the body caused by acute myocardial infarction. The success of prevention and treatment of VF depends on the early hospitalization of acute myocardial infarction patients in specialized intensive care and resuscitation units where emergency reanimation measures can be taken, controlled therapy rendered, and VF prevented by influencing the altered metabolism and stress state. Special attention is paid to repeated VF for which the authors employ, along with routine therapy, Glucagon that produces an antiarrhythmic and cardiotonic effect.
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PMID:[Therapy and prevention of different forms of ventricullar fibrillation in myocardial infarct]. 87 Jul 39

In non-obese, non-diabetic patients suffering acute myocardial infarction, angina pectoris, previous myocardial infarction and peripheral vascular disease, the plasma levels of glucose, insulin, C-peptide and glucagon were determined in basal condition and during an intravenous glucose tolerance test. In the four groups there was a high frequency of glucose intolerance. Basal hyperinsulinism was present in all groups; in groups; in those which maintained normal glucose tolerance there was a high B-cell response to the sugar. Basal hyperglucagonemia was found in the early stage of acute ischemic heart disease, in patients with previous myocardial infarction and in those with peripheral vascular disease. The elevated plasma glucagon levels may play a role in the complex disturbance of carbohydrate metabolism present in patients with atherosclerotic vascular disease.
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PMID:Carbohydrate metabolism and plasma levels of insulin and glucagon in patients with atherosclerotic vascular disease. 304 64

1. In anaesthetized dogs, glucagon (100 mug/kg i.v.), caused a significant increase in heart rate and decrease in mean arterial blood pressure. Ventricular automaticity, as determined by the time to the onset of first vagal escape beat and the number of such indioventricular beats during the 30 s period of vagal stimulation, was not significantly altered.2. In unanaesthetized dogs with ventricular arrhythmias produced by two-stage ligation of the anterior descending branch of the left coronary artery, glucagon (30 and 100 mug/kg i.v.), restored normal sinus rhythm in a few animals. In the remaining dogs, there was a significant reduction in the ventricular ectopic activity.3. The significant positive chronotropic response to glucagon elicited in anaesthetized animals was not observed in conscious dogs whose coronary arteries had been ligated.4. These findings enhance the potential usefulness of glucagon in the treatment of acute myocardial infarction, which may often be associated with disturbances of ventricular rhythm.5. In the light of observations made by other workers, it is suggested that the antiarrhythmic effect of glucagon may be due to movement of potassium ions into the cardiac cell.
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PMID:Effect of glucagon on ventricular arrhythmias after coronary artery occlusion and on ventricular automaticity in the dog. 515 98

Glucagon was administered to six patients with acute myocardial infarction. Three of them had cardiogenic shock syndrome. Glucagon produced a positive inotropic response in all cases, which resulted in a significant rise in blood pressure, with only slight chronotropic effect. No arrhythmias were induced, and all patients with cardiogenic shock improved temporarily. Further evaluation of glucagon in shock syndrome to determine the dose and method of administration is required.
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PMID:Glucagon and haemodynamics of acute myocardial infarction. 535 22

The central and peripheral vascular haemodynamic effects of glucagon were studied in 29 patients. With a single dose method of 2 or 5 mg. glucagon intravenously the inotropic action of the drug produced immediate increased myocardial contractility with significant increase in cardiac output and enhanced cardiac performance, and lowering of pulmonary arterial pressure and pulmonary vascular resistance. No primary peripheral vascular effect was evident, and the increased systemic pressure and lowered systemic resistance appear to be secondary to the central action of the drug. With the dosage used there were no undesirable side-effects apart from a feeling of slight nausea. Though the haemodynamic effects are abrupt, reaching their maximum values in the first 10 minutes after injection, they tend to be dissipated within half an hour, presumably due to the very rapid destruction of the drug. Repeated booster doses rather than continuous infusion may be the method of choice to maintain an increased cardiac output. The positive chronotropic action of the drug may cause transient palpitations. Glucagon increased the cardiac output in the acute phase of myocardial infarction by 42 per cent. The haemodynamic effects in chronic rheumatic heart disease are more varied, and it may increase left atrial pressure in mitral stenosis, which is undesirable. Hyperglycaemia results from liver glycogenolysis but blood sugar levels rarely exceeded 200 mg./100 ml. These results warrant further study of the value of glucagon as a positive inotropic agent in low output heart failure, especially in acute myocardial infarction with cardiogenic shock, or after cardiac surgery, or in unrelieved chronic congestive heart failure.
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PMID:Haemodynamic effects of glucagon. 542 74

We have recently demonstrated the benefits of glucagon-like peptide-1 (GLP-1) in enhancing regional and global myocardial function after reperfusion in the clinical setting of acute myocardial infarction. We hypothesized that GLP-1 facilitates recovery from myocardial stunning after an ischemic event. To investigate this, we administered GLP-1 (1.5 pmol/kg/min) to six dogs undergoing 10-min occlusion of the left circumflex coronary artery, followed by 24-h reperfusion. We compared the responses of coronary blood flow and regional thickening of the posterior wall with a group of eight vehicle-treated dogs undergoing the same occlusion-reperfusion protocol. Although recovery of coronary blood flow was identical, regional wall motion recovery occurred significantly ((*)p < 0.05) earlier (92 +/- 4 versus 57 +/- 5%(*) at 15 min) and was complete in the GLP-1-treated dogs, whereas residual contractile dysfunction persisted in the control group (99 +/- 4 versus 78 +/- 3%(*) at 24 h). This phenomenon was independent of changes in systemic hemodynamics or global systolic function. However, isovolumic left ventricular relaxation improved significantly in GLP-1-treated dogs. GLP-1 caused an insulinotropic effect, but no hypoglycemia. We conclude that GLP-1 enhances recovery from ischemic myocardial stunning after successful reperfusion.
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PMID:Glucagon-like peptide-1 limits myocardial stunning following brief coronary occlusion and reperfusion in conscious canines. 1535 13

Glucagon-like peptide 1 (GLP-1) was discovered as an incretin (insulinotropic gut) hormone. Biological actions of GLP-1 in healthy and type 2 diabetic subjects include (a) stimulation of insulin secretion in a glucose-dependent manner, (b) suppression of glucagon, (c) reduction in appetite and food intake, (d) deceleration of gastric emptying. In animal experiments, in addition, (e) stimulation of beta-cell neogenesis, growth and differentiation in animal and tissue culture experiments, and (f) in vitro inhibition of beta-cell apoptosis induced by different agents have been observed. Since the incretin effect--the higher insulin secretory response to oral as compared to intravenous glucose loads - is reduced in patients with Type 2 diabetes, GLP-1 has been used to pharmacologically replace incretin. Intravenous GLP-1 can normalise, and subcutaneous GLP-1 can significantly lower plasma glucose in the majority of patients with Type 2 diabetes. The magnitude of this effect does not greatly depend on patient characteristics such as age, sex, obesity, or baseline insulin and glucagon, with minor influences of previous antidiabetic therapy and actual metabolic control. GLP-1 itself, however, is inactivated rapidly in vivo by the protease DPP IV and can only be used for short-term metabolic control, such as in intensive care units (potentially useful in patients with acute myocardial infarction, coronary surgery, cerebrovascular events, septicaemia, during the perioperative period and while on parenteral nutrition). For more long-term metabolic control, incretin mimetics (agonists at the GLP-1 receptor) with more favourable pharmacokinetic profiles should be used.
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PMID:Glucagon-like peptide 1 (GLP-1) in the treatment of diabetes. 1565 19

We have shown previously that the glucagon-like peptide-1 (GLP-1)-(7-36) amide increases myocardial glucose uptake and improves left ventricular (LV) and systemic hemodynamics in both conscious dogs with pacing-induced dilated cardiomyopathy (DCM) and humans with LV systolic dysfunction after acute myocardial infarction. However, GLP-1-(7-36) is rapidly degraded in the plasma to GLP-1-(9-36) by dipeptidyl peptidase IV (DPP IV), raising the issue of which peptide is the active moiety. By way of methodology, we compared the efficacy of a 48-h continuous intravenous infusion of GLP-1-(7-36) (1.5 pmol.kg(-1).min(-1)) to GLP-1-(9-36) (1.5 pmol.kg(-1).min(-1)) in 28 conscious, chronically instrumented dogs with pacing-induced DCM by measuring LV function and transmyocardial substrate uptake under basal and insulin-stimulated conditions using hyperinsulinemic-euglycemic clamps. As a result, dogs with DCM demonstrated myocardial insulin resistance under basal and insulin-stimulated conditions. Both GLP-1-(7-36) and GLP-1-(9-36) significantly reduced (P < 0.01) LV end-diastolic pressure [GLP-1-(7-36), 28 +/- 1 to 15 +/- 2 mmHg; GLP-1-(9-36), 29 +/- 2 to 16 +/- 1 mmHg] and significantly increased (P < 0.01) the first derivative of LV pressure [GLP-1-(7-36), 1,315 +/- 81 to 2,195 +/- 102 mmHg/s; GLP-1-(9-36), 1,336 +/- 77 to 2,208 +/- 68 mmHg] and cardiac output [GLP-1-(7-36), 1.5 +/- 0.1 to 1.9 +/- 0.1 l/min; GLP-1-(9-36), 2.0 +/- 0.1 to 2.4 +/- 0.05 l/min], whereas an equivolume infusion of saline had no effect. Both peptides increased myocardial glucose uptake but without a significant increase in plasma insulin. During the GLP-1-(9-36) infusion, negligible active (NH2-terminal) peptide was measured in the plasma. In conclusion, in DCM, GLP-1-(9-36) mimics the effects of GLP-1-(7-36) in stimulating myocardial glucose uptake and improving LV and systemic hemodynamics through insulinomimetic as opposed to insulinotropic effects. These data suggest that GLP-1-(9-36) amide is an active peptide.
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PMID:Active metabolite of GLP-1 mediates myocardial glucose uptake and improves left ventricular performance in conscious dogs with dilated cardiomyopathy. 1602 74


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