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Query: UNIPROT:P01275 (glucagon)
26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the metabolism and hormone profile of 9 patients with moderately severe acute asthma before treatment, and again 10 min after intravenous aminophylline (250 mg) or the selective beta-adrenergic stimulant hexoprenaline (5 microgram) intravenously. Compared with basal values in normal subjects the untreated asthmatics had statistically significant raised mean plasma pancreatic glucagon, free fatty acid (FFA) and glucose levels in the plasma and a significantly depressed mean plasma potassium level. Insulin, growth hormone, cortisol, thyrotropin and ketone body levels were normal. The only significant changes after therapy were a further fall in plasma potassium in the hexoprenaline-treated patients and a rise in the mean lactate concentration of the group as a whole. The clinical implications of these findings are briefly considered.
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PMID:Metabolic studies in acute asthma before and after treatment. 43 79

We investigated the effect of intravenous infusions of aminophylline on plasma glucose, insulin (IRI), glucagon (IRG), growth hormone (HGH), cortisol, and free fatty acid (FFA) levels in healthy young subjects. Six received an intravenous loading dose of aminophylline (6.0 mg/kg over 20 min) followed by a maintenance dose (0.9 mg/kg/hr) for 100 min. Another 7 subjects initially received smaller loading (3.0 mg/kg) and maintenance (0.45 mg/kg/hr) doses, and after 60 min they received a second loading dose (3.0 mg/kg) followed by a larger maintenance dose (0.9 mg/kg/hr) over 120 min. In these fasting volunteers, infusion of aminophylline, which produced theophylline levels in the usual therapeutic range (10 to 20 microgram/ml) caused small increases in plasma glucose levels without changing IRI, IRG, HGH, or cortisol. There were rapid, pronounced, and prolonged rises in FFA associated with the aminophylline infusion. Increases in FFA paralleled the rise in theophylline levels. It is concluded that routine therapeutic doses of theophylline, i.e., doses that achieve serum levels normally encountered in treatment for bronchial asthma, cause a marked rise in FFA and a slight rise in glucose (8 +/- 3 mg/dl) without changing levels of IRI, IRG, HGH, or cortisol.
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PMID:Metabolic responses to plasma concentrations of theophylline. 44 67

Patients manifesting intrinsic idiopathic rhinitis and/or asthma in association with diabetes or aspirin intolerance were studied. Various metabolites (sugars and L-histidine) and chemical (aspirin, insulin and glucagon) challenges were studied using the parameter of the induced sequential vascular response. A standard oral glucose tolerance test was also correlated. The results indicated similar as well as divergent ab- nc. nalities of responses to the various carbohydrates, insulin, glucagon, L-histidine and aspirin challenges. This permitted a separation of some patients with idiopathic rhinitis and/or asthma into those associated with diabetes and those with tolerance to aspirin.
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PMID:Intrinsic asthma associated with diabetes mellitus; abnormal vascular response and glucose tolerance tests. 112 56

Severe asthma and diabetes have been reported not to co-exist in the same patient. Various studies have attributed this to the possible association of asthma with hyperinsulinism, increased responsiveness to insulin or to beta-blockade. Previous studies have not addressed all these possible mechanisms in the same patient. In this prospective study, 7 atopic asthmatics and 7 age and sex-matched healthy controls underwent glucose, insulin and glucagon tolerance tests. The results showed no evidence of hyperinsulinism or increased responsiveness to insulin. Intravenous administration of glucagon, however, showed a lesser increase of glucose and insulin in asthmatics. Since glucagon has a beta-agonist effect on the liver and activates glycogenolysis and gluconeogenesis via beta-receptor stimulation and stimulates insulin secretion by activating adenylate cyclase of pancreatic beta-cells through beta-receptors, the results of glucagon tolerance test in our study may therefore suggest the presence of partial beta-blockade in atopic asthmatics.
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PMID:Glucose metabolism and beta receptor function in atopic asthmatics. 136 92

Twenty-five patients with acute severe asthma were treated with oxygen, corticosteroids and either salbutamol or aminophylline by intravenous infusion. Blood glucose, plasma insulin and glucagon were measured during the first 24 hours of treatment. Salbutamol and aminophylline rapidly caused hyperglycaemia, accompanied by a rise in insulin and a fall in plasma glucagon. At first the increase in plasma insulin was insufficient to restore normoglycaemia, but by 24 hours homeostasis was restored. The early submaximal insulin response was attributed to the fasting caused by breathlessness. There was no evidence of an increase in hormone secretion caused by direct beta 2-adrenergic stimulation of the pancreatic islets. The effect of corticosteroids on blood glucose over the period of study was considerably less than the contribution of either salbutamol, or aminophylline.
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PMID:Mechanisms of abnormal glucose metabolism during the treatment of acute severe asthma. 143 70

Although there have been several reports of adverse reactions to contrast material during barium gastrointestinal (GI) studies, these are considered highly unusual. During a 27-month period at the author's institution, seven reactions to contrast material occurred during 6,918 colon examinations, and four reactions to contrast material occurred during 11,534 upper GI procedures. This frequency is greater than what has been reported previously. Most reactions were fairly mild, with urticaria and pruritus, although two patients, both with a history of asthma, had severe reactions that required emergency treatment. One patient had similar adverse reactions during both upper and lower GI examinations. Since only two patients received glucagon, this is not believed to be a factor. It is likely that patients react to some additive in the barium suspension. The radiologist must be aware of these complications and be ready to begin appropriate treatment.
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PMID:Increased frequency of reactions to contrast materials during gastrointestinal studies. 239 33

Glucagon, an activator of cyclic AMP that produces smooth muscle relaxation, was studied to determine if it had the ability to reverse or modify the degree of bronchospasm in asthmatic patients. Fourteen patients with mild to moderately severe bronchospastic exacerbation of asthma were studied using peak expiratory flow rates (PEFR) before and after receiving one milligram of glucagon intravenously. Eight (57%) of the 14 patients demonstrated a mean PEFR increase of 113 L/min ten minutes following glucagon administration and were termed responders. This study suggests that further investigation of the role of glucagon in asthmatic patients is warranted.
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PMID:Glucagon as a therapeutic agent in the treatment of asthma. 236 12

During a one-month period, two cases of beta-adrenergic blocker overdose were treated by the emergency staff at our hospital. One case of propranolol intoxication demonstrated profound cardiovascular collapse and generalized tonic-clonic seizures. The condition failed to respond to high-dose intravenous pressor agents, but did improve significantly with IV glucagon infusion. The second overdose involved atenolol. Although the blood levels reported were very high, the patient showed no cardiovascular compromise and required only inhaled bronchodilators for an exacerbation of her asthma.
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PMID:Beta blocker overdose with propranolol and with atenolol. 285 42

We evaluated the effect of glucagon on eight patients with asthma. After withholding bronchodilators for 12 hours, patients received either 2 units of intravenous glucagon or 2 ml of saline after a double-blind crossover protocol. Glucagon significantly improved the FEV1 (17.5% +/- 5.5 SEM) and the peak expiratory flow rate (14.2% +/- 4.9), compared to placebo (-2.4% +/- 2.9, p less than 0.02; 4.5% +/- 4.1, p less than 0.25, respectively). Seven patients had an excellent response to glucagon (40% to 105% of the response to inhaled isoproterenol), but four patients had no significant response. We conclude that glucagon, through its pharmacologic actions, can have a bronchodilator effect in selected patients with asthma.
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PMID:A bronchodilator action of glucagon. 337 10

The stress response in humans commonly includes elevations in plasma concentrations of glucocorticoids, catecholamines, glucagon, growth hormone, aldosterone, and renin, resulting in alterations in the metabolism of glucose and other energy substrates, and in increased sodium and water retention. In severe illness, triiodothyronine and sometimes thyroxine are decreased without evidence of clinical hypothyroidism. Antidiuretic hormone may be elevated in bacterial meningitis and other central nervous system disorders, as well as in acute asthma, chronic ventilator therapy, pneumothorax, atelectasis, and postoperatively. Increased ADH concentration can lead to significant hypoosmolality and hyponatremia with adverse effects on the patient. In the setting of severe intracerebral insults, ADH may be inappropriately low, resulting in diabetes insipidus. Insulin concentrations may be inappropriately low for serum glucose concentration, or insulin may have diminished receptor responsiveness in seriously stressed patients. Either situation leads to hyperglycemia. Disturbances in calcium, phosphorus, and magnesium homeostasis may occur relatively frequently in the critically ill patient in response to therapeutic interventions, or illness-induced altered metabolism. It is not always clear when an altered metabolic or hormonal state is an appropriate response to a stress, or represents decompensation of the body's mechanisms for coping with that stress. It is important, however to recognize the common responses of the organism to severe illness, and to monitor for treatable abnormalities which occur.
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PMID:Endocrine manifestations of critical illness in the child. 354 20


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