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)

A study of seven patients, each of whom was treated with dopamine within three hours after suffering a myocardial infarction. For four of these, a comparative study was made with isoproterenol, glucagon and ouabaine. The average age of the subjects was 72 years, and all presented considerable myocardial lesions before the treatment was begun. Despite improvement, particularly in diuresis and cardiac output, none of the patients survived. The authors explain these results by the fact that, like all powerful inotropic agents, dopamine produces an increase in oxygen consumption of the myocardium for the ischemic cells situated in the zone contiguous to the infarct.
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PMID:[Use of dopamine in the treatment of cardiogenic shock. Preliminary results]. 0 34

The effects of isolated and combined use of strophanthin and glucagon on the values of central hemodynamics and cardiac contractile function were compared. The study was conducted on patients with myocardial infarction complicated by congestive heart failure in the acute period of the disease. It was found that a combination of these drugs had a synergic inotropic effect. A conclusion was drawn on the advantages of the combined use of strophanthin and glucagon in the treatment of severe congestive heart failure in the acute period of myocardial infarction.
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PMID:[Combined use of glucagon and strophanthin in myocardial infarct complicated by severe cardiac insufficiency]. 34 97

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

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

The blood levels of glucagon, growth hormone and glucose were investigated in early (1st day) and late stages (3rd week) of myocardial infarction in 11 cases of severe and 6 cases of mild myocardial infarction. The results were related to those in 9 healthy controls. In severe myocardial infarction associated with complications the glucagon level was statistically significantly higher than in controls in the early as well as in the late stage of the disease. In mild myocardial infarction this was not observed. The growth hormone level was significantly higher than normal in patients with severe myocardial infarction in only a few cases and only in the early stage. The differences between both stages of infarction and between patients and controls were not significant. Blood glucose level in the early stage of severe myocardial infarction was higher than normal and statistically significantly higher than in the late stage. In view of the differences in blood glucose and glucogon levels during severe myocardial infarction it seems that hyperglycemia in early stages of the disease depends on the high catecholamines level in the blood and on the insulin: glucagon index and not on the absolute concentration of glucagon in the blood.
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PMID:Relationship between the blood glucagon, growth hormone and glucose levels in myocardial infarction. 99 57

Data derived from a study into the efficacy of glucagon in 50 patients with acute and chronic cardiac insufficiency are offered. In all of these cases there existed a grave cardiac insufficiency refractory to therapy with cardiac glycosides, mostly attended by deranged rhythm and conduction. Clinical and instrumental investigations (basic hemodynamic indices established through the dye-dilution method and integral rheography, polycardiography) proved glucagon to be a truly cardiotonic agent in dealing with patients of this category. A greater effect was achieved in cases involving acute cardiac insufficiency associated with myocardial infarction than it could be obtained in instances of a long-standing chronic decompensation. The use of glucagon is particularly indicated in cases when cardiac glycosides produce complications, or cannot be employed due to the already existent derangements of the rhythm and conduction.
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PMID:[Use of glucagon in cardiac insufficiency]. 123 16

Plasma levels of a variety of hormones have been measured in patients within two hours of the onset of symptoms of myocardial infarction and before commencement of any treatment. Increased plasma concentrations were found for norepinephrine, epinephrine, glucagon, aldosterone, vasopressin, atrial natriuretic peptide, corticotrophin, prolactin, cortisol and substance P while plasma renin activity was raised. The plasma concentrations of insulin, growth hormone, neurotensin, bombesin and vasointestinal peptide were normal.
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PMID:Hormonal response in untreated myocardial infarction. 210 97

The mechanisms underlying the non-competitive beta-antagonistic properties of amiodarone were investigated, and the haemodynamic responses to exercise following the administration of oral amiodarone or intravenous propranolol were compared in dogs with a healed myocardial infarction submitted to a graded treadmill exercise. In radioligand binding studies, amiodarone, up to 10 mumol/L did not compete with 125I-iodocyanopindolol for binding to rat heart beta-adrenoceptors. Exposure of cardiac membranes to greater concentrations of amiodarone induced a significant decrease in the number of beta-adrenoceptors without affecting their affinity for 125I-iodocyanopindolol. Similar results were observed ex vivo, in rats after single or multiple dose administration. When added in vitro to rat heart membranes, amiodarone non-competitively inhibited the activation of adenylate cyclase by isoprenaline, glucagon and secretin. Stimulation of adenylate cyclase by those agents which act at more internal sites in the sarcolemmal membrane such as GppNHp, sodium fluoride or forskolin, was much less affected by amiodarone. In dogs performing at a submaximal work level, amiodarone significantly reduced heart rate and tended to increase coronary flow and to reduce left ventricular end-diastolic pressure, but did not affect left ventricular dP/dt. During submaximal exercise, propranolol had similar effects on heart rate, but dramatically reduced myocardial contractility.
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PMID:Amiodarone. Biochemical aspects and haemodynamic effects. 298 37

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


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