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)

Administration of tyramine (with or without phentolamine) as well as induction of ether anesthesia or insulin hypoglycemia caused a sharp increase in plasma cyclic AMP in rats. Based on the findings that the treatment of rats with reserpine, 6-hydroxydopamine, cocaine or propranolol totally abolished tyramine-induced increases in plasma cyclic AMP, it was concluded that catecholamines released from sympathetic neuronal terminals by tyramine could activate adenylate cyclase via the stimulation of postsynaptic beta-adrenoceptors. In contrast, catecholamines secreted from adrenal medulla were largely responsible for the increase in plasma cyclic AMP induced by ether anesthesia; whereas glucagon, in addition to adrenal catecholamines, played a significant role in hypoglycemia-induced increases in plasma cyclic AMP. Assay of plasma cyclic AMP following these stimuli is very promising as a test for adrenergic activities in experimental and clinical studies.
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PMID:Increases in plasma cyclic AMP dependent on endogenous catecholamines. 20 22

Direct cardiac and vascular effects of the antikaliuretic diuretic potassium-canrenoate were measured in cardio-surgical patients during extracorporal circulation and immediatly after operations, each time in neuroleptanalgesia. During "steady state" extracorporeal circulation (aorta cross-clamped, constant flow rate of heart-lung-machine, constant hypothermia), in 13 patients no significant influence on peripheral circulation was found after i.v.-injection of 800 mg potassium-canrenoate. Neither arterial perfusion pressure (representing an arterial vascular reaction) nor changes in oxygenator-volume (indicating venous vasodilation or contraction) demonstrated significant differences in comparison to a control group. After cardiac surgery haemodynamic measurements were performed for a period of 60 minutes in 10 patients given 800 mg potassium-canrenoate. In comparison with a control group (n = 6), no significant differences in arterial pressure, heart rate, cardiac index and pulmonary arterial pressure were found. Left ventricular measurements, using a catheter tip manometer, revealed no direct positive inotropic effect of a single i.v.-injection of potassium-canrenoate. In acute myocardial failure during anaesthesia or in "low cardiac ouptut" following open heart surgery no improvement in myocardial contractility is obtained by i.v.-application of potassium-canrenoate; at the present there seems no alternative to other positive inotropic agents such as calcium, glucagon, dopamine, orciprenaline and epinephrine.
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PMID:[Extrarenal effects of potassium-canrenoate. Haemodynamic investigations during neuroleptanalgesia in cardiosurgical patients (author's transl)]. 31 42

Injection of streptozotocin in newborn rats induced a severe diabetic syndrome on day 4 after birth, with acute hyperglycaemia and glycosuria. Over the next 3 weeks spontaneous recovery occurred as attested by normal basal blood glucose and plasma insulin levels. Recovery was, however, incomplete in the adult since a definite impairment in insulin release and glucose disposal was observed. This state was characterized by the following features: 1) a 72% decrease in pancreatic insulin stores without change in pancreatic glucagon stores; 2) a slight but consistent elevation of blood glucose in the fasted and fed basal states and especially of blood glucose 90 min after an IV glucose load (2 g/kg) performed under pentobarbitone anaesthesia; 3) a considerable decline in the glucose-induced insulin release with a decrease in the maximal response. Both early and late phases of insulin release were impaired, as indicated by in vivo glucose infusion experiments. Basal plasma glucagon levels were normal. Over a period of 12 months with a normal laboratory diet no aggravation of the chemical diabetic state was observed. This new experimental syndrome is a potentially interesting model for the study of the influence of environmental factors on the development of overt diabetes.
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PMID:Chemical diabetes in the adult rat as the spontaneous evolution of neonatal diabetes. 39 4

Oral glucose tolerance tests were performed under pentobarbital anesthesia in 43 male Wistar rats 2 to 18 months of age in order to determine if insulin and glucagon secretion are altered with aging. Although any linear correlation was not demonstrated between aging and blood glucose, plasma insulin or glucagon levels, post-glucose levels of blood glucose were significantly suppressed and those of plasma glucagon were significantly elevated at 4 to 6 months of age. No significant difference was found between young (2 months of age) and aged rats (12 to 14 and 17 to 18 months of age) in either blood glucose or plasma insulin levels during oral glucose load. On the other hand, post-glucose plasma glucagon levels of the aged rats were significantly higher than those of the young ones. Furthermore, comparisons of various kinds of indices among the different age groups, such as insulinogenic index, insulin/glucagon and so forth during oral glucose tolerance tests also indicate the significant alteration of glucagon secretion during aging process. It is concluded from the present data that glucose tolerance does not apparently deteriorate during aging process in rats but that glucagon responses to oral glucose administration are elevated with aging.
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PMID:Insulin and glucagon relationships during aging in rats. 47 20

A newly developed artificial pancreatic beta cell is described and its use in five children with diabetes mellitus is evaluated. This device can be programmed to bring the blood glucose concentration rapidly to a preselected level and normalize glucose tolerance in juvenile diabetic patients with markedly different insulin requirements. It is portable, can be operated by one person, and has been used to regulate the blood glucose concentration before, during, and after surgery requiring general anesthesia. The potential value of the device as an investigational tool is shown by demonstrating that regulation of the blood glucose concentration with insulin for seven to 24 hours does not alter circulating glucagon concentrations in the juvenile diabetic patients studied.
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PMID:Clinical evaluation and preliminary studies on the use of an artificial pancreatic beta cell in juvenile diabetes mellitus. 56 36

The effect of the administration of anti-insulin serum to newborn rats, surgically delivered under ether anaesthesia at term, was examined with respect to liver glycogen concentration and plasma concentrations of glucose, lactate and free fatty acids. Newborn rats thus treated showed decreased liver glycogen concentrations and elevated plasma concentrations of glucose, lactate and free fatty acids compared to untreated control animals one hour later. These effects were dose-dependent with respect to the amount of anti-insulin serum administered. The simultaneous administration of glucagon with anti-insulin serum at birth was no more effective in mobilising glycogen stores than anti-insulin serum alone, although plasma glucose concentrations in these animals were higher and plasma lactate concentrations were lower. Either anti-insulin serum or glucagon abolished the postnatal hypoglycaemia observed in untreated neonatal rats. The rate of fall in plasma lactate concentrations after birth was stimulated in glucagon-treated rats but was retarded in rats treated with anti-insulin serum. Hormonal control over the initiation of glycogenolysis and gluconeogenesis in the newborn rat appears to be different, a fall in plasma insulin being the prime factor involved in triggering glycogen mobilization and a rise in plasma glucagon the prime event that initiates gluconeogenesis.
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PMID:Glucose metabolism in the newborn rat: the role of insulin. 62 34

1. Pancreatic and adrenal responses to intense hypoxia have been examined in conscious unrestrained calves 3-5 weeks after birth. 2. The outputs of both cortisol and corticosterone from the right adrenal gland rose steadily in response to hypoxia and this cortical secretory response was accompanied by a pronounced increase in blood flow through the gland. The changes in both steroid output and adrenal blood flow corresponded with those which occur in response to supramaximal doses of corticotrophin in calves of the same age. 3. Neither adrenaline nor noradrenaline were released in significant amounts from the adrenal medulla until the arterial PO2 had fallen below 15 mmHg. Such severe hypoxia caused secretion of catecholamines at rates comparable with those recorded during maximal stimulation of the sympathetic innervation to the gland in anaesthetized calves. The response to intense hypoxia in these conscious calves differed from that which occurs under anaesthesia in that the amount of adrenaline released was invariably greater than that of noradrenaline. 4. Severe hypoxia produced a rapid but transient increase in plasma glucagon concentration, followed by a pronounced rise in plasma glucose concentration in animals with abundant liver glycogen. No change in plasma insulin concentration was observed during hypoxia although it rose subsequently in response to hyperglycaemia. 5. Bilateral section of the splanchnic nerves virtually abolished the release of catecholamines in response to hypoxia but the adrenal cortical and pancreatic responses did not appear to be affected.
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PMID:Adrenal and pancreatic endocrine responses to hypoxia in the conscious calf. 78 61

Blood glucose and serum potassium (K+) concentrations were measured before, during, and 60 minutes after operation in two groups of 10 patients during nitrous oxide/halothane/d-tubocurarine anesthesia for major orthopedic surgery. In the control group, arterial blood pressure was maintained within normal range, while in the study group trimethaphan camsylate was administered as an intravenous infusion (average, 218 mg.) to maintain a systolic blood pressure of 60 to 65 torr. In the normotensive group, blood glucose rose significantly during operation and early postoperatively and serum K+ was essentially unchanged. In the hypotensive group, trimethaphan caused a striking modification of surgically induced hyperglycemia, together with a small significant decrease in serum K+ intraoperatively. The observed increase in blood glucose is part of the autonomic response to surgical stress. Hormonal factors (growth hormone, cortisol and glucagon) may conceivably be involved. The decrease in serum K+ is probably caused by decreased hepatic glycogenolysis and attenuation of the suppressive effect of catecholamines on insulin release, both effects being secondary to the ganglionic blocking property of trimethaphan. These results indicate that trimethaphan, in contrast to other ganglionic blocking drugs, does not cause hypoglycemia and suggest that serum K+ concentration should be monitored whenever these drugs are used.
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PMID:Changes in serum potassium and blood glucose concentrations after trimethaphan administration in man. 93 27

The effect of intravenous injection of 50 mug/kg of glucagon on the hepatic circulation of the pig was studied in 12 animals. Glucagon caused an arterial pressure reduction of 11 mm Hg after two minutes and 7 mm Hg after ten minutes. The portal pressure and blood flow were not altered. The superior mesenteric arterial flow decreased by 12%. The hepatic arterial blood flow increased by 80% after two minutes and by 58% after ten minutes. There was no difference in response when anesthesia was achieved with small intravenous doses of thiopental (Pentothal) sodium or 70% nitrous oxide in oxygen and tubocurarine chloride.
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PMID:Effect of glucagon on hepatic circulation in the pig. 99 4

The systolic time intervals and calculated parameters of PEP/LVET (pre-injection period/left ventricular ejection time-ratio) and 1/PEP2 before and after induction of anaesthesia with the barbiturate enibomal (Narcodorm) were studied noninvasively in eight surgical patients after pre-treatment with a bolus dose of glucagon. The mean difference between the PEP/LVET-ratio before and after induction was 0.06, and the mean difference between 1/PEP2 before and after induction was -8. The corresponding values in the control group consisting of 12 patients were 0.09 and -28, respectively, suggesting a somewhat greater depression of cardiac function in this group. However, no statistically significant difference at the 5% level was found between changes in the glucagon group and controls. The influence of barbiturates and glucagon on cardiac function is discussed.
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PMID:Influence of glucagon on systolic time intervals during induction of anaesthesia with barbiturate. 118 7


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