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)

We report a case of a 17 year old sports woman, who had a ventricular fibrillation episode with cardiogenic shock during endonasal anaesthesia containing epinephrine. She was so transferred to our department (in shock): the 2-D echo showed biventricular hypokinesia without dilatation (LVEF less than 25%). Endomyocardial biopsy performed 5 days later showed active lymphocyte myocarditis with interstitial fibrosis. There were serum antibodies anti-Echo 9 and Coxsackie B 1, 2, 3. Immunoassay, urinary catecholamines and glucagon test were normal. The clinical picture was resolved within 15 days using intravenous isoprenaline and/or dopamine initially followed by oral diuretics and digoxin; the therapy was broke off at the time of discharge. We believe that the vasoconstriction and/or the oxygen wasting effect caused by epinephrine revealed latent myocarditis which had not been shown up even by intensive physical training.
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PMID:[Acute latent myocarditis appearing with ventricular fibrillation after intranasal administration of adrenaline. Description of a case]. 260 90

We investigated the effects of sevoflurane anesthesia and of surgery, on the endocrine functions as reflected by plasma levels of cortisol, aldosterone, ACTH, beta-endorphin-like immunoreactivity, prolactin, insulin, growth hormone, glucagon and glucose in surgical patients.
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PMID:Endocrine evaluation of sevoflurane, a new inhalation anesthetic agent. 262 72

Previous studies demonstrated that insulin-induced hypoglycemia enhances glicentin secretion in piglets and prompted us to investigate the response of glucagon-like immunoreactivity (GLI) to hypoglycemia in dogs. Insulin hypoglycemia did not induce any rise of plasma total immunoreactive glucagon (IRG) measured by nonspecific antiserum to glucagon in normal or pancreatectomized dogs under anesthesia. In contrast, insulin-induced hypoglycemia clearly increased plasma total IRG in both normal and pancreatectomized dogs in a conscious state. Administration of acetylcholine resulted in an elevation of plasma total IRG, whereas epinephrine induced a slight increase in plasma total IRG. The infusion of alpha- or beta-adrenergic blockers did not affect the response of plasma total IRG to hypoglycemia, whereas atropine completely blunted the increase in plasma total IRG during insulin hypoglycemia. Similarly atropine abolished the rise of plasma total IRG during intravenous administration of 2-deoxy-D-glucose. It is concluded that hypoglycemia clearly enhances the secretion of GLI from the gut in dogs and that GLI secretion during hypoglycemia is modulated, at least in part, by the autonomic nervous system.
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PMID:Response of gut glucagon-like immunoreactivity to hypoglycemia in dogs. 264 47

We studied whether insulin and glucagon secretory capacities change in relation to the corresponding hormonal contents in the pancreas remnant after pancreas resection. The following groups of dogs were used: sham operated (S-O), left pancreatectomized (L-Px), right pancreatectomized (R-Px), subtotal pancreatectomized (St-Px), and total pancreatectomized (T-Px). Endocrine functions were assessed by intravenous glucose tolerance test (IVGTT) and insulin tolerance test (ITT) in each dog under anesthesia before surgery and 1 wk after. In these five groups, the insulin secretory capacities, assessed as the integrated incremental secretion of immunoreactive insulin (sigma delta IRI) from the IVGTT, decreased to 95 +/- 11, 78 +/- 9, 48 +/- 8, 12 +/- 8, and -4 +/- 4% of the respective preoperative values, and these values were proportional to the percentage residual weight (100, 64 +/- 2, 35 +/- 2, 13 +/- 2, 0%) and IRI content (100, 59 +/- 4, 45 +/- 3, 10 +/- 2, 0%) of the pancreas remnant. After surgery, glucagon secretory capacity, the integrated incremental secretion of immunoreactive glucagon (sigma delta IRG) during the ITT, decreased significantly in the L-Px, St-Px, and T-Px groups but not in the R-Px group. The sigma delta IRG values as percentages of the preoperative values were 109 +/- 25, 46 +/- 11, 89 +/- 13, 19 +/- 11, and 3 +/- 3%, respectively, for the five groups. These values were proportional to the percentage residual IRG contents of the pancreas remnants (100, 48 +/- 6, 65 +/- 8, 12 +/- 2, 0%) rather than to the percentage residual pancreatic weights.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin and glucagon secretion after pancreatectomies. Correlation of secretion and hormonal contents of remaining pancreas. 266 Dec 85

Anesthesia, surgery, and hypothermia are conventionally considered the major stress factors in the metabolic and hormonal responses to cardiac surgery. We compared these responses in 14 nondiabetics during and for 24 h after coronary artery bypass surgery; 8 received cardioplegic solutions (C+), and 6 did not (C-). The mean intraoperative glucose load in C+ was 106 g compared to 32 g in C-; postoperatively both groups received 50 g. Marked hyperglycemia (31.8 +/- 4.8 mmol/L) occurred during hypothermia in C+, but dropped to 18.9 mmol/L before surgery ended and to 11.2 +/- 1.1 mmol/L by 2 h postop. In contrast, C- showed constant mild hyperglycemia of 8.3-9.8 mmol/L throughout, significantly less than C+ until 1 h postop. Insulin was suppressed by 55% only during hypothermia, peaking with rewarming in C+ at 2,849 +/- 911 vs. 639 +/- 251 pmol/L in C- (P less than 0.05); as with glycemia, values were comparable after 2 h postop. The pancreatic beta-cell thus responded to hyperglycemia during restoration of normothermia, resulting in a rapid decline in glycemia. This occurred despite elevations in antiinsulin factors in both groups; GH was 14 +/- 4 micrograms/L, cortisol was 607 +/- 38.6 nmol/L, norepinephrine was 11.5 +/- 3.7 nmol/L, epinephrine was 13,863 +/- 3,875 pmol/L, and FFA were 0.36 +/- 0.05 g/L. Early postop, a secondary rise in stress hormones occurred in both groups. Maximal cortisol values were at 4 h (1,186 +/- 140 nmol/L) and peaks of norepinephrine (6.50 +/- 1.66 nmol/L), epinephrine (7,969 +/- 3,602 pmol/L), and FFA (0.27 +/- 0.03 g/L) occurred. The only significant glucagon elevation was at 24 h (C+, 464 +/- 53 ng/L; C-, 350 +/- 241 ng/L; P less than 0.02), Thus, 1) many metabolic responses during coronary artery bypass surgery are influenced by the glucose-containing cardioplegic solution; 2) hypothermia suppresses insulin secretion, but it responds thereafter despite marked elevations of catecholamines, and is associated with decreasing glycemia despite elevated antiinsulin factors; 3) a lesser but highly significant stress response corresponds to awakening from anesthesia; and 4) glucagon plays a minor role in intraoperative hyperglycemia; the rise at 24 h is unexplained.
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PMID:Hormonal and metabolic responses during coronary artery bypass surgery: role of infused glucose. 267 36

Polyethylene tubes were inserted into the bile duct and femoral vein of rats under pentobarbital anaesthesia and bile was collected for three 2-h periods. After the first (control) period the animals were infused intravenously at a rate of 1.2 ml/h with the following compounds: (1) 0.9% (w/v) NaCl (control group), (2) glucagon (1200 ng/h), (3) vasopressin (1200 ng/h) or (4) angiotensin II (600 ng/h). The concentrations of thyroxine (T4), tri-iodothyronine (T3) and reverse tri-iodothyronine (rT3) in the bile were estimated by radioimmunoassay. No significant differences between groups were found in the biliary excretion of T4 and T3, while the excretion of rT3 after the infusion of all the hormones used was significantly (P less than 0.001 at 2 to 4 h of the infusion) increased, no such increase being found in the controls. It may be concluded therefore that the administration of the above hormones resulted in some changes in iodothyronine metabolism in the liver. These may be explained by an inhibition of iodothyronine 5'-monodeiodination related to the glycogenolytic and gluconeogenetic effects of these hormones.
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PMID:Effect of the glycogenolytic gluconeogenetic hormones, glucagon, vasopressin and angiotensin II, on biliary excretion of iodothyronines in rats is possibly related to the inhibition of 5'-monodeiodination in the liver. 275 63

Protein catabolism following injury is associated with elevated levels of the stress hormones cortisol, glucagon, and the catecholamines. To study the effect of hormonal blockade on catabolic responses to surgery, 16 dogs underwent general anesthesia, a standard abdominal operation, and implantation of aortic and caval catheters. Five received phentolamine and propranolol continuously, at doses which block catecholamine effects. To prevent the rise in both catecholamines and cortisol, 6 received a high epidural anesthetic (T4-S3), started preoperatively and continued for 24 hr. Five dogs served as controls. Hindquarter amino acid flux was measured at 6 and 24 hr post-op. Pre- and post-op skeletal muscle biopsies were analyzed for amino acids. Urinary nitrogen was measured over 24 hr. Urinary nitrogen excretion was unaffected by treatment, but urinary creatinine fell from 0.039 +/- 0.002 g/24 hr X kg for controls to 0.03 +/- 0.002 for the epidural group and 0.031 +/- 0.001 for alpha and beta blockade (P less than 0.05). Hindquarter amino acid nitrogen efflux was decreased from -19.05 +/- 4.06 mumole/min X kg in controls to -8.98 +/- 0.86 in the epidural and -6.89 +/- 1.21 in the alpha- and beta-blockade groups (P less than 0.05). The urinary nitrogen loss, glutamine efflux, and fall in muscle glutamine produced by the operation were not prevented by either form of hormonal blockade, but hindquarter nitrogen efflux was diminished. Hormonal blockade inhibits net skeletal muscle protein catabolism without altering whole-body nitrogen loss. Hormones and other factors must be responsible for the increased ureagenesis that occurs following injury.
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PMID:Hormonal blockade modifies post-traumatic protein catabolism. 286 76

In a randomised controlled trial, preterm babies undergoing ligation of a patent ductus arteriosus were given nitrous oxide and d-tubocurarine, with (n = 8) or without (n = 8) the addition of fentanyl (10 micrograms/kg intravenously) to the anaesthetic regimen. Major hormonal responses to surgery, as indicated by changes in plasma adrenaline, noradrenaline, glucagon, aldosterone, corticosterone, 11-deoxycorticosterone, and 11-deoxycortisol levels, in the insulin/glucagon, molar ratio, and in blood glucose, lactate, and pyruvate concentrations were significantly greater in the non-fentanyl than in the fentanyl group. The urinary 3-methylhistidine/creatinine ratios were significantly greater in the non-fentanyl group on the second and third postoperative days. Compared with the fentanyl group, the non-fentanyl group had circulatory and metabolic complications postoperatively. The findings indicate that preterm babies mount a substantial stress response to surgery under anaesthesia with nitrous oxide and curare and that prevention of this response by fentanyl anaesthesia may be associated with an improved postoperative outcome.
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PMID:Randomised trial of fentanyl anaesthesia in preterm babies undergoing surgery: effects on the stress response. 2092 62

Overall glucose uptake represents the sum of insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). In this study, we compared the rate of NIMGU in conscious and anesthetized dogs. Rates of glucose disposal were compared in the basal state and during severe insulinopenia after endogenous insulin suppression by high-dose somatostatin (SRIF) infusion. Steady-state NIMGU rates were calculated 2 h after commencing SRIF infusion. Three groups of studies were performed: 1) SRIF in conscious dogs; 2) SRIF in anesthetized dogs; and 3) SRIF plus glucagon, also in anesthetized dogs. In all three groups, serum insulin levels were reduced to below assay sensitivity after SRIF infusion. The basal metabolic clearance rate of glucose (MCRg) for each group was 3.8 +/- 0.4, 3.6 +/- 0.3, and 3.6 +/- 0.3 ml X kg-1 X min-1, respectively (P = NS, all groups). Steady-state NIMGU rates were 2.4 +/- 0.2 (conscious), 2.5 +/- 0.1 (anesthetized, SRIF only), and 2.4 +/- 0.1 ml/kg/min (anesthetized, SRIF plus glucagon). Thus, absolute rates of NIMGU expressed as MCRg in conscious and anesthetized animals do not differ and in the three groups studied comprise approximately the same proportion of the basal glucose uptake (approximately 64, approximately 69, and approximately 66%, respectively). We conclude that approximately 66% of basal postabsorptive glucose uptake occurs via NIMGU mechanisms and that this pathway is unaffected by anesthesia and surgery.
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PMID:Non-insulin-mediated glucose uptake predominates in postabsorptive dogs. 288 96

Biological activities of highly potent octapeptide analogs of somatostatin (SS), D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) and D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121), were investigated in male rats. When analog RC-160 was administered to rats in which serum growth hormone (GH) levels were elevated by pentobarbital anesthesia, a dose-related inhibition of GH was obtained at dose range of 0.1 to 2.5 micrograms/kg. The time course of GH inhibition by RC-160, RC-121 and SS-14 was studied in rats treated with phenobarbital, morphine and chlorpromazine. Analogs RC-160 and RC-121 induced a prolonged inhibition of GH levels, in contrast to SS-14, whose effect was short-lived. The analogs suppressed the GH level for more than 2 hr, the peak inhibition being seen 30 to 60 min after the injection. The effects of analogs RC-160 and RC-121 on insulin secretion were observed in rats, in which insulin levels had been elevated by intravenous administration of glucose (500 mg/rat). Administration of RC-160 suppressed insulin secretion, dose-dependently, maximum but not complete inhibition being achieved at a dose of 100 micrograms/kg. In this model, RC-160 and RC-121, in doses of 30 micrograms/kg, induced a similar inhibition of insulin release as 200 micrograms/kg of SS-14, whose action of SS-14 was transient. The effect of analog RC-160 on glucagon release was studied in rats with glucagon levels elevated by hypoglycemia. RC-160 suppressed the secretion of glucagon, the inhibition being dose-dependent in the range of 0.1 to 2 micrograms/kg. Doses of 2 and 10 micrograms/kg of this analog completely suppressed the hypoglycemia-induced glucagon release. These results indicate that analogs RC-160 and RC-121 possess prolonged and enhanced biological activities, the former analog showing a high selectivity in inhibiting GH and glucagon release in vivo as compared with that of insulin secretion.
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PMID:Effects of highly potent octapeptide analogs of somatostatin on growth hormone, insulin and glucagon release. 288 86


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