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 case of refractory hypotension following propranolol overdose is reported. Management included isoprenaline, glucagon and extracorporeal circulatory support using femoral vein-femoral artery bypass. The unreliability of neurological observations, especially unreactive pupils, in the presence of drug overdose is reiterated.
Anaesthesia 1991 Sep
PMID:Extracorporeal circulation in the management of massive propranolol overdose. 156 14

To assess the role of the central nervous system (CNS) in carbohydrate metabolism in diabetes, neostigmine was injected into the third cerebral ventricle in fed rats with streptozotocin (STZ; 80 mg/kg)-induced diabetes under pentobarbital sodium anesthesia. Changes in hepatic venous plasma glucose concentrations were monitored. Neostigmine injection caused no significant changes in the hepatic venous plasma glucose concentration in untreated diabetic rats, whereas the glucose level increased significantly in insulin-treated diabetic rats similarly to the changes in normal control animals. In diabetic rats, the plasma levels of glucagon, epinephrine, and norepinephrine were increased significantly by neostigmine. After various doses (35-80 mg/kg) were given to rats, it was found that the higher the STZ dose, the lower was the hepatic glycogen content and the smaller was the glycemic response to neostigmine. Our results indicate that, in severe diabetes, CNS stimulation with neostigmine fails to increase hepatic glucose output, because glycogen stores are nearly exhausted and gluconeogenesis is already maximal.
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PMID:CNS stimulation does not affect hepatic venous glucose concentration in severely diabetic rats. 200 97

Anesthetic experience with three cases of the resection of glucagonoma, a rare tumor of alpha cells of pancreatic islets, is presented. Marked increases of blood glucagon and glucose levels, with the potential for clinically significant metabolic and myocardial dysfunction, did not occur during anesthesia and surgery. Associated tumors of other endocrine cell types also were absent in the three study patients. Strategies for anticipating and managing other perioperative problems associated with glucagonoma also are discussed.
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PMID:Anesthesia for glucagonoma resection. 200 43

To define the vagal circuitry mediating the cephalic phase insulin response (CPIR), this reflex was measured in conscious, freely moving rats that had previously undergone selective abdominal vagotomies that spared different columnar subpopulations of dorsal motor nucleus of the vagus (dmnX) neurons. The CPIR was defined as an increase of plasma insulin from basal at 2 min after the start of ingestion. The CPIR measured in peripheral blood after chow ingestion was reliable and significant (P less than 0.05) in rats with all branches intact, +24.9 +/- 5.1 microU/ml (+130% increase from basal); rats with only the two gastric branches and the hepatic branch intact, +27.0 +/- 3.5 microU/ml (+153%); and rats with only the hepatic branch intact, +13.5 +/- 4.8 microU/ml (+188%). No significant response occurred in animals with only the two celiac branches intact, +1.8 +/- 1.8 microU/ml (+15%) or in those with none of the branches intact, +3.9 +/- 3.3 microU/ml (+21%). The CPIRs measured in portal vein blood were generally larger but showed the same pattern across groups. Plasma glucose measurements of portal vein blood indicated that with chow ingestion no significant absorption had occurred by 2 min, whereas with either milk or glucose intake absorption did occur. Subsequent bilateral electrical cervical vagal stimulation-induced insulin and glucagon responses in the same animals under anesthesia showed the same branch dependency. It is concluded that the CPIR is mediated by the two gastric and the hepatic branches but not the two celiac vagal branches. The perikarya of the preganglionics innervating the pancreatic B-cells are contained within a large pool occupying the two medial columns of the dmnX.
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PMID:Identification of vagal preganglionics that mediate cephalic phase insulin response. 217 54

We studied the influence of prolonged anaesthesia and surgery on glucose metabolism by means of the euglycaemic insulin clamp method in eight patients who underwent prolonged surgery. Eleven patients who underwent surgery of short duration served as a control group. Plasma concentrations of catabolic hormones were measured simultaneously. Glucose utilization during prolonged anaesthesia, (PA) group, was lower than that in the control group (P less than 0.01) (glucose utilization 7.59 +/- 0.73 mg.kg-1.hr-1 in the control group vs 4.03 +/- 0.71 mg.kg-1.hr-1 in PA group respectively). There were no significant differences in plasma catecholamine and glucagon concentrations between the PA and control groups. Plasma-free fatty acid levels increased significantly in the PA group before the euglycaemic insulin clamp (free fatty acid level: 0.496 +/- 0.053 mmol.L-1 in the control group, vs 0.834 +/- 0.103 mmol.L-1 in the PA group at the pre-clamp period, P less than 0.01). Tissue resistance to exogenous insulin increased during prolonged anaesthesia and surgery although there were no significant changes in plasma catabolic hormone levels.
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PMID:Decreased glucose utilization during prolonged anaesthesia and surgery. 220 35

We have previously shown that iv glucagon improved survival in rats from 33 to 83% when given after, but not during, superior mesenteric artery (SMA) occlusion. This study investigated potential hemodynamic mechanisms of this effect. In Part 1, cardiac output (CO) was measured in 12 male Sprague-Dawley rats with an electromagnetic flow-probe that had been placed around the ascending aorta 5 days previously. Under pentobarbital anesthesia, the SMA was occluded for 85 min. All rats received normal saline (NS, 15 ml/kg/hr) for 1 hr before and after SMA declamping. Control rats (n = 6) received only NS. Treated rats (n = 6) received NS plus glucagon (1.6 micrograms/kg/min iv) for 1 hr postocclusion. CO decreased 50% during the first hour after SMA declamping in control rats, but only 11% in glucagon-treated rats (P less than 0.02). Systemic vascular resistance (SVR) increased by 90% in control rats by 1 hr after declamp, but only 9% in glucagon rats (P less than 0.04). Systemic blood pressure and heart rate were not different in the two groups. In Part 2, relative distribution of visceral blood flow was measured with radiolabeled microspheres injected in the aortic root before clamping, before declamping, and 1 hr postdeclamping in 10 rats (5 glucagon, 5 control) using the above protocol. After SMA clamping, the proportion of visceral blood flow distributed to the intestine fell from 45 to 20% (P less than 0.05). During reperfusion, the proportion of intestinal flow exceeded baseline (P less than 0.05), but was not different in control (64%) and glucagon-treated rats (56%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of glucagon after acute mesenteric ischemia in rats. 221 46

The changes in arterial ketone body ratio (acetoacetate/beta-hydroxybutyrate) were investigated in 7 patients undergoing hepatectomy under epidural anesthesia with nitrous oxide and oxygen. The plasma levels of glucose, insulin, glucagon, lactate, pyruvate and non-esterified free fatty acid (NEFA) were measured during the operation. The plasma level of insulin activity increased significantly during surgery. The secretory capability of insulin against glucose load was relatively preserved. Arterial ketone body ratio also increased during the operation. The plasma insulin activity was positively correlated significantly with the arterial ketone body ratio (Y = 0.98 + 0.76X; r = 0.76). Both lactate and pyruvate increased significantly during surgery. No remarkable changes of L/P ratio reflecting the redox state in cytoplasma were found in both groups. Our results suggest that the quantity of glucose load and insulin activity should be considered when arterial ketone body ratio is measured during the operation.
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PMID:[Clinical study of arterial ketone body ratio (ACAC/beta-OHCS) during hepatectomy]. 234 91

Plasma glucose, insulin, glucagon, free fatty acid, ketone body, lactate and pyruvate were measured in 14 patients undergoing gastrectomy under general anesthesia with nitrous oxide and oxygen. Lactated ringer solution with glucose load (10 g.hr-1) was administered in seven patients [glucose loading group: Glucose (+)] and the other seven patients received only lactated ringer solution [glucose free group: Glucose (-)]. Blood glucose increased significantly in both groups, but a significant difference appeared between Glucose (+) and Glucose (-). Plasma insulin activity and IRI/BS ratio increased in Glucose (+) and a significant difference was found between the two groups. No remarkable change in plasma glucagon level was found in both groups. Free fatty acid and ketone bodies (acetoacetate, beta-hydroxybutyrate) decreased significantly in Glucose (+), but they increased significantly in Glucose (-) and significant differences were found between the two groups. The rate of changes of beta-hydroxybutyrate was consistently higher than that of acetoacetate. Lactate and pyruvate increased significantly in both groups. These results suggest that continuous glucose loading may facilitate insulin release from the pancreas and suppress the hyperketonemia and hyperlipidemia during partial gastrectomy.
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PMID:[The effect of glucose loading on changes in ketone and glucose metabolism during gastrectomy]. 236 42

Previous studies have indicated that motor center ("feedforward") activity is important for hormonal and metabolic responses to exercise. Now, epidural blockade at vertebrae L3-L4 was used to evaluate the importance of afferent neural feedback from working muscles. Six healthy, young males cycled for 20 min at 55 +/- 4% (mean +/- SE) of maximal oxygen uptake with, as well as without, epidural anesthesia. During anesthesia cutaneous sensory blockade was present below segment T11-12, the postexercise ischemic pressor response was attenuated from 34 +/- 9 to 14 +/- 4 mmHg, muscle strength reduced to 80 +/- 5% of control, and perceived exertion (Borg scale) was increased. At rest hormonal and metabolic parameters did not change in response to epidural anesthesia. During exercise, responses of catecholamines, insulin, glucagon, and growth hormone (GH) in plasma as well as glucose production and utilization, plasma free fatty acids, and plasma glycerol were similar in epidural and control experiments (P greater than 0.05). In contrast during submaximal exercise, plasma concentrations of adrenocorticotropin (ACTH) and beta-endorphin increased only in experiments without epidural anesthesia. The data indicate that impulses in afferent nerves from the working muscles are essential for the ACTH and beta-endorphin responses to submaximal dynamic exercise in humans. Afferent nervous activity is probably less important than efferent activity from motor centers for responses of GH, catecholamines and insulin, and, in turn, extramuscular fuel mobilization in exercise.
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PMID:Hormonal and metabolic responses to exercise in humans: effect of sensory nervous blockade. 254 39

Recent studies suggest that, in addition to classical humoral metabolic feedback mechanisms, the mobilization of glucoregulatory hormones and glucose in exercise may be regulated by motor centers in the brain. We, therefore, studied the effect of electrically stimulating the posterior hypothalamic locomotor region (PHLR) for 10 min in decorticated (n = 6) and alpha-chloralose-anesthetized (n = 8) cats. Blood pressure and heart rate were measured, and blood samples were drawn for analysis of hormones and metabolites before, during, and after 10 min of PHLR stimulation. Feedback from contracting muscles was prevented by neuromuscular blockade in decorticated cats and by the anesthesia in anesthetized cats. In decorticated cats, PHLR stimulation elicited increases (2 P less than 0.05) in glucose production (delta 54 +/- 16 mumol.min-1.kg-1), plasma glucose (delta 2.2 +/- 0.7 mmol/l), epinephrine (delta 4.9 +/- 1.8 pmol/l), norepinephrine (delta 2.2 +/- 0.9 pmol/l), glucagon (delta 16 +/- 5 pmol/l), decreases (2 P less than 0.05) in plasma insulin (delta 27 +/- 7 pmol/l), and increases (2 P less than 0.05) in blood pressure (delta 48 +/- 9 mmHg) and heart rate (delta 26 +/- 7 beats/min). In anesthetized cats, PHLR stimulation elicited increases (2 P less than 0.05) in glucose production (delta 12 +/- 4 mumol.min-1.kg-1), plasma glucose (delta 0.4 +/- 0.1 mmol/l), blood pressure (delta 39 +/- 7 mmHg), and heart rate (delta 28 +/- 7 beats/min), whereas changes in catecholamine and insulin concentrations did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mobilization of glucoregulatory hormones and glucose by hypothalamic locomotor centers. 259


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