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

The efficacy of beta adrenergic blocking agents has been observed in the treatment of a variety of cardiac arrhythmias. Electrophysiological experiments demonstrated that beta receptor blocking drugs prevent catecholamine-induced alterations of the transmembrane action potential. Clinically used beta blocking agents are effective in preventing arrhythmias provoked by sympathetic stimulation such as sinus tachycardia, paroxysmal junctional tachycardia, atrial, nodal, and ventricular premature contractions. Beta receptor blocking drugs are especially useful in tachycardias based on hyperkinetic heart syndrome and in exercise-induced premature beats in patients suffering from coronary heart disease. Beta blocking agents are--at least in our hands--most useful in combination with class I antiarrhythmic drugs with the intention to reduce the dosage--i.e. the side effects--of various antiarrhythmic drugs. In hyperthyroidism beta adrenergic blocking agents are effective complementary to the specific treatment. In cases of intoxication with beta blocking drugs complicated by myocardial depression and severe bradycardia glucagon must be regarded as a very useful compound.
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PMID:[Spectrum of effects of beta receptor blockade in cardiac arrhythmias]. 243 70

The effect of mixidine fumarate on myocardial chronotropic responses to various stimulants was examined. Mixidine decreased elevated heart rate in the anesthetized dog to basal levels. It produced a dose-related decrease in heart rate elevated reflexly by aminophylline, by beta adrenergic stimulation induced by isoproterenol, by sympathetic nerve stimulation and by intravenous infusion of glucagon. Mixidine attenuated the increase in contractile force produced by sympathetic nerve stimulation but not that induced by isoproterenol. The compound antagonized the increase in rate of isolated guinea-pig atria induced by both isoproterenol and histamine. In the conscious dog, mixidine caused no decrease in resting heart rate, mean arterial pressure and cardiac output. It reduced atropine-induced sinus tachycardia as well as that induced by treadmill exercise. Experiments in the dog heart-lung preparation indicated that attenuation of an epinephrine-induced sinus tachycardia led to a decrease in myocardial oxygen consumption and an increase in myocardial efficiency. These studies suggest that mixidine fumarate induces an antichronotropic activity by a direct effect on the sinoatrial node and by attenuating sympathetic nervous system input to the heart.
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PMID:Cardiovascular profile of mixidine fumarate, a compound which attenuates myocardial chronotropic responses. 735 51

Calcium channel blockers (CCB) and beta-blockers (BB) account for approximately 40% of cardiovascular drug exposures reported to the American Association of Poison Centers. However, these drugs represent >65% of deaths from cardiovascular medications. Yet, caring for patients poisoned with these medications can be extremely difficult. Severely poisoned patients may have profound bradycardia and hypotension that is refractory to standard medications used for circulatory support.Calcium plays a pivotal role in cardiovascular function. The flow of calcium across cell membranes is necessary for cardiac automaticity, conduction and contraction, as well as maintenance of vascular tone. Through differing mechanisms, CCB and BB interfere with calcium fluxes across cell membranes. CCB directly block calcium flow through L-type calcium channels found in the heart, vasculature and pancreas, whereas BB decrease calcium flow by modifying the channels via second messenger systems. Interruption of calcium fluxes leads to decreased intracellular calcium producing cardiovascular dysfunction that, in the most severe situations, results in cardiovascular collapse.Although, CCB and BB have different mechanisms of action, their physiological and toxic effects are similar. However, differences exist between these drug classes and between drugs in each class. Diltiazem and especially verapamil tend to produce the most hypotension, bradycardia, conduction disturbances and deaths of the CCB. Nifedipine and other dihydropyridines are generally less lethal and tend to produce sinus tachycardia instead of bradycardia with fewer conduction disturbances.BB have a wider array of properties influencing their toxicity compared with CCB. BB possessing membrane stabilising activity are associated with the largest proportion of fatalities from BB overdose. Sotalol overdoses, in addition to bradycardia and hypotension, can cause torsade de pointes. Although BB and CCB poisoning can present in a similar fashion with hypotension and bradycardia, CCB toxicity is often associated with significant hyperglycaemia and acidosis because of complex metabolic derangements related to these medications. Despite differences, treatment of poisoning is nearly identical for BB and CCB, with some additional considerations given to specific BB. Initial management of critically ill patients consists of supporting airway, breathing and circulation. However, maintenance of adequate circulation in poisoned patients often requires a multitude of simultaneous therapies including intravenous fluids, vasopressors, calcium, glucagon, phosphodiesterase inhibitors, high-dose insulin, a relatively new therapy, and mechanical devices. This article provides a detailed review of the pharmacology, pathophysiology, clinical presentation and treatment strategies for CCB and BB overdoses.
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PMID:Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity. 1589 28