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)

Local anaesthetic systemic toxicity is a rare but often dramatic complication of regional anaesthesia. Convulsions often follow warning signs, easily recognized when looked for; but they may occur from the first. They are rapidly followed by hypoxia and hypercapnia which greatly enhance the risk of severe cardiac depression, mainly with bupivacaine or etidocaine. Thiopentone is able to stop convulsions quickly, but may further depress the cardiovascular system. Diazepam has been shown to be effective in the treatment of local anaesthetic-induced convulsions. It gives less myocardial depression, but is much slower in effect. Midazolam, a new short-acting benzodiazepine, should be the best choice. Should tracheal intubation become necessary, suxamethonium can be used. Indeed, the principal use of these drugs is to make ventilation easier, so as to restore rapidly correct oxygenation. Severe cardiac depression, often leading to cardiac arrest, may occur from the first or after the appearance of convulsions. It generally follows a regional block carried out with bupivacaine. A few antiarrhythmic drugs have been used to treat ventricular arrhythmias, either in experimental studies (lidocaine, bretylium) or after clinical accidents (lidocaine). Their efficacy and innocuity have to be proved before they can be proposed to treat these accidents. Bradycardia only needs treatment with atropine when it causes severe haemodynamic disturbances. When cardiac arrest occurs, cardiopulmonary resuscitation must be carried out; its mainstays are: oxygen, sodium bicarbonate, adrenaline, calcium and perhaps glucagon. This must be continued for a long time, as late successes have been published.
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PMID:[How should a toxic accident be treated?]. 290 Jun 15

To assess whether specific peptidases regulate neuropeptide disposition, we have examined histochemically the localization of dipeptidyl-aminopeptidase II (DAP II). With beta-naphthylamide (beta-NA) substrates, this enzyme has a selectivity for lysyl-alanyl-beta-NA. DAP II staining is highly localized to specific neuronal populations with no staining over glia. Areas in the brain with high densities of DAP II staining include the mitral cells in the olfactory bulb, polymorphic cells in the hippocampus, the paraventricular nucleus of the hypothalamus, and the anterior dorsal thalamus, Purkinje cells, and deep nuclei in the cerebellum. Staining occurs in virtually all cell groups in the inferior colliculus, red nucleus, oculomotor nucleus, and mesencephalic nucleus of the trigeminal nerve, the stratum album of the superior colliculus, as well as most cells in the cochlear and superior olivary nuclei. DAP II localizations do not correlate fully with those on any known neuropeptide. Of the numerous peptides evaluated, only glucagon competes substantially for the DAP Ii substrate, reducing enzymatic activity by 50% at a 2 x 10(-5) M concentration.
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PMID:Brain peptidase with a unique neuronal localization: the histochemical distribution of dipeptidyl-aminopeptidase II. 702 39

Between 1972 and 1978, a total of 159 cases of esophageal foreign body were treated at the University of Minnesota Affiliated Hospitals, Minneapolis. Although coins were the most frequent offending agent in the pediatric group, meat was the most common in the entire series (60%). Eighty percent of coins were impacted in the upper esophagus, while meat impaction occurred most frequently in the distal esophagus (42%). Rigid esophagoscopy was performed in 134 patients. The foreign body was removed during esophagoscopy in 122 cases, advanced into the stomach in two cases, and not found in ten cases. In addition to esophagoscopy, when meat obstruction was suspected, several pharmacologic agents were successful in relieving the obstruction, such as parenterally administered diazepam (Valium) (8/27) and glucagon (6/14). Spontaneous passage was noted in seven cases. No cases of esophageal carcinoma were discovered in this series.
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PMID:Current management of esophageal foreign bodies. 721 86

Diazepam suppressed arginine-induced glucagon release from the isolated perfused rat pancreas in a dose-dependent manner, with an IC50 of approximately 65 microM. In contrast, insulin release was enhanced by 10-50 microM diazepam, but inhibited by higher concentrations of drug. Thus, 50 microM diazepam simultaneously suppressed glucagon and increased insulin release in this model. The potentiation of insulin release may result from phosphodiesterase inhibition. The inhibitory effects on hormone release are discussed in terms of diazepam's molecular conformation, which is similar to that of diphenylhydantoin, an inhibitor of both glucagon and insulin release in the isolated perfused rat pancreas. The possibility is also considered that the conformation of both compounds might be similar to the apparent active site of the hormone release inhibitor somatostatin.
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PMID:Diazepam: in vitro effects on glucagon and insulin release. 1562 63

We investigated the vascular effects of glucagon-like peptide-1 (GLP-1) and Exendin-4 in type 2 diabetic rat aortae. Studies were performed in a normal control group (NC) (0.2 ml i.p. saline, n = 10), streptozotocin (STZ)/nicotinamide diabetic control group (DC) (a single dose of 80 mg/kg STZ i.p. injection 15 min after administration of 230 mg/kg nicotinamide i.p.), GLP-1 (GLPC) control group (1 microg/kg twice daily i.p. for 1 month, n = 10), Exendin-4 control group (EXC) (0.1 microg/kg twice daily i.p. for 1 month, n = 10), GLP-1-treated diabetic group (GLPT) (1 microg/kg twice daily i.p. for 1 month, n = 10), and Exendin-4-treated diabetic group (EXT) (0.1 microg/kg twice daily i.p. for 1 month, n = 10). One month of GLP-1 and Exendin-4 treatment significantly decreased the blood glucose levels of diabetic rats (113 +/- 2 mg/dl, p < 0.001, and 117 +/- 1 mg/dl, p < 0.001, respectively versus 181 +/- 9 mg/dl in the DC group). Sensitivity (pD2) and maximum response (% Max. Relax) of acetylcholine-stimulated relaxations in the DC group (pD2: 6.73 +/- 0.12 and 55 +/- 6, respectively) were decreased compared with the non-diabetic NC group (pD2: 7.41 +/- 0.25, p < 0.05, and 87 +/- 4, p < 0.01). Treating diabetic rats with GLP-1, pD2 values and with Exendin-4, Max. Relax %values of aortic strips to acetylcholine returned to near non-diabetic NC values (pD2: 7.47 +/- 0.15, p < 0.05, and 87 +/- 3, p < 0.01, respectively). Maximal contractile responses (Emax) to noradrenaline in aortic strips from the diabetic DC group (341 +/- 27 mg tension/mg wet weight) were significantly decreased compared with the non-diabetic NC (540 +/- 66 mg tension/mg wet weight, p < 0.001) and the GLPT group (490 +/- 25 mg tension/mg wet weight, p < 0.05). There were no significant differences in pD2 values of aortic strips to noradrenaline from all groups. Emax to KCl in aortic strips from the DC group (247 +/- 10 mg tension/mg wet weight, p < 0.01) was significantly decreased compared with non-diabetic NC group (327 +/- 26 mg tension/mg wet weight). Treating diabetic rats with GLP-1 (GLPT), Emax values of aortic strips to KCl returned to near non-diabetic NC values (271 +/- 12 mg tension/mg wet weight). GLP-1 and (partially) Exendin-4 treatment could improve the increased blood glucose level and normalize the altered vascular tone in type 2 diabetic rats.
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PMID:Effect of glucagon-like peptide-1(7-36) and exendin-4 on the vascular reactivity in streptozotocin/nicotinamide-induced diabetic rats. 1574 70