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)

The work demonstrates the efficacy of glucagon in acute myocardial infarction and its complications, particularly in bradycardia, hypotension, disorders of cardiac rhythm and conduction, cardiogenic shock, cardiac insufficiency in complete atrioventricular heart block and recurrent forms of ventricular fibrillation. A differential approach and dynamic control over the effect of the drug on the values of hemodynamics, respiration, and metabolism are necessary under the conditions of units of intensive therapy and cardioresuscitation.
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PMID:[Differential use of glucagon in acute period of myocardial infarct]. 31 54

A 26-year old woman took 4000 mg (100 tablets) of VerpamilR (Orion Pharmaceutica, Helsinki) with suicidal intestions. As a consequence of the poisoning cardiogenic shock, 3rd grade AV block and cardiac arrest occurred. The disturbance of stimulus formation and conduction was treated with a temporary pacemaker. Discussing the therapeutical possibilities it is stated that cardiovascular symptoms may be influenced successfully by Ca++ preparations (Calcium gluconicum, Calcium chloratum) and beta-receptor stimulants (isoproterenol, dopamine, orciprenalin) possibly also with glucagon.
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PMID:[Attempted suicide with verapamil]. 265 56

Acute poisoning with beta adrenergic inhibitors is rare although such drugs are widely prescribed. Between 1966 and 1980, 40 cases were recorded at the Fernand-Widal Toxicology Center. 40% of patients were asymptomatic and 25% had sinus bradycardia. 35% of patients had specific toxic signs, either atrioventricular block (20%) or hemodynamic disorders (15%); the latter were seen only when associated heart disease was present or when another cardiotropic agent had been absorbed. No deaths were recorded. This favorable prognosis may result from the self-limited nature of poisoning with beta blocking agents, myocardial function being similar to that which follows denervation. In severe cases, management includes pacing and glucagon.
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PMID:[Beta adrenergic receptor blockade : a self-limited phenomenon explaining the benignancy of acute poisoning with beta adrenergic inhibitors. Report of a series of 40 patients seen at the Fernand-Widal Toxicology Center, with a 0% mortality rate (author's transl)]. 612 35

We report the case of 52-year-old woman, who ingested 3.6 g of diltiazem, 16 g of potassium chloride and 6.5 g of magnesium, in a suicide attempt 4 hours before admission. She developed cardiorespiratory failure, with severe hypotonia and acute renal failure, in ECG third degree atrioventricular block was stated. The highest potassium concentration was 8.0 mmol/l, magnesium 2.15 mmol/l. As a result of multiple pharmacologic intervention, including intravenous fluids, calcium, glucagon, dopamine, dobutamine, norepinephrine, transvenous pacing and peritoneal dialysis (haemodynamic instability makes haemodialysis noneffective) the haemodynamic stabilization of cardiovascular system and normalization of potassium and magnesium concentration were achieved. The diltiazem concentration was measured using liquid chromatography, the result was 0.89 microgram/ml. She was discharged in a good clinical condition on day 26th.
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PMID:[Severe mixed poisoning with diltiazem, potassium and magnesium: a case report]. 1456 97

The morbidity and mortality of a severe calcium channel blocker intoxication is high due to serious toxic cardiac effects. Its treatment is supported by low-quality evidence from the heterogeneous literature. We describe a case of a severe diltiazem intoxication and critically appraise the efficacy and role of high-dose calcium and glucagon infusions. A 53-year-old woman was admitted to the emergency department with a cardiogenic shock with complete AV block, not responding to atropine, isoprenaline and an external pacemaker. Later on, it became clear that she had a severe diltiazem intoxication which was successfully treated with isotone fluids, inotropes, vasopressors and continuous infusion of high-dose calcium and glucagon. The patient developed, however, an acute, necrotizing pancreatitis, probably related to iatrogenic high calcium levels. This case demonstrates lack of consensus regarding target levels of serum calcium for treatment of a severe diltiazem intoxication. Goal-directed tapering of calcium should prevent side effects of iatrogenic hypercalcaemia. The contribution of glucagon infusions is doubtful due to the instability of solubilized glucagon. This might explain why the effect of glucagon is variable in the literature.
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PMID:A Critical Note on Treatment of a Severe Diltiazem Intoxication: High-Dose Calcium and Glucagon Infusions. 2850 40