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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary heart disease is the most common cause of death in many Westernized countries. Patients who experience either a threatened myocardial infarction (MI) or an acute MI within the last 12 h or so can benefit from interventions that decrease myocardial oxygen demand. Beta-Blockade fulfills such a purpose mainly through diminishing the product of heart rate x systolic blood pressure. Added benefits of beta-blockade include (a) a redistribution of myocardial blood supply in favour of ischaemic areas, (b) inhibition of catecholamine-induced myocardial necrosis, and (c) a decrease in the Q-Tc interval and an increase in the threshold to ventricular fibrillation. Beta 1-Selective blockade is the essential ingredient; the possession of intrinsic sympathomimetic activity (ISA) may diminish benefit. Intravenous, followed by oral, beta-blockade within 12 h (preferably 6 h) of the onset of chest pain results in (a) a marked reduction in chest pain, (b) a reduction in infarct size by about 30%, (c) a diminished likelihood of threatened infarction progressing to overt infarction, (d) a reduction in the number of life-threatening ventricular arrhythmias, and (e) a reduction in the incidence of cardiac arrest and reinfarction. Intravenous, followed by oral, beta 1-selective blockade (atenolol) significantly reduces vascular mortality by about 15% at 1 week post-MI, and the benefit is maintained at 1 year. Such an intervention, provided contraindications to beta-blockade are respected, is safe and well tolerated. Probably about 50% of patients are eligible for such treatment. Such an approach is highly cost effective.
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PMID:Beta-blockade in acute myocardial infarction. 246 37

The effect of epinephrine and norepinephrine on myocardial oxygen delivery and consumption during cardiopulmonary resuscitation using open cardiac massage after a 5-min period of electrically induced ventricular fibrillation was studied in 21 pigs with a mean body weight of 21 kg. Norepinephrine, like epinephrine, is a sympathomimetic agent with marked alpha- and beta-1-sympathomimetic activity, but the degree of beta-2-stimulation is less marked than that obtained with epinephrine. After mechanical measurements over 3 min (compression rate = 60/min), 7 animals received 10 ml physiological saline, 7 further animals, 45 micrograms/kg epinephrine, and the remaining 7 animals, 45 micrograms/kg norepinephrine. At 90 s and again at 5 min after the administration of epinephrine or norepinephrine, the mean arterial blood pressure was significantly higher than in the control group, while mean pulmonary artery pressure, central venous pressure and cardiac index were not significantly different. Total myocardial blood flow was only measured before the induction of cardiac arrest in the control group, where it was found be 193 +/- 30 ml/min/100 g. During the open cardiac massage but before the injection of catecholamines we found a myocardial blood flow of 51 +/- 23 in the control group, 71 +/- 10 in the epinephrine group, and 74 +/- 11 ml/min/100 g in the norepinephrine group. At 90 s after the injection, blood flow increased by 78% to 126 +/- 18, with epinephrine and by 45%, to 107 +/- 30 ml/min/100 g tissue with norepinephrine. At 5 min after administration of these catecholamines significant differences from the control group were present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of adrenaline and noradrenaline on the oxygen supply of the myocardium during cardiopulmonary resuscitation]. 273 21

1. The initial effect of bretylium tosylate on isolated rabbit atria was to increase conduction velocity, contraction heights, spontaneous frequency and maximum driven frequency, and to reduce electrical threshold. At concentrations of 200 mg/l. or less, these were the only effects, and were consistent with the known sympathomimetic actions of bretylium.2. At extremely high concentrations, 1,200 and 2,400 mg/l., the initial actions were succeeded by weak quinidine-like effects; reduced conduction velocity, spontaneous and maximum driven frequencies, and rate of rise of action potential. The electrical threshold was raised, but contraction heights were not reduced.3. The local anaesthetic activity of bretylium, measured by reductions in the frog nerve action potential, was 1/90 that of procaine and 1/300 that of propranolol, on a molar basis.4. Acute pretreatment with bretylium, 20 mg/kg intravenously, significantly increased the amount of infused ouabain required before the appearance of the first signs of atrial arrhythmia in anaesthetized guinea-pigs, but did not prevent ventricular arrhythmias.5. Pretreatment with bretylium 30 mg/kg subcutaneously 24 hr, and again 4 hr before ouabain infusion, increased the dose of ouabain inducing atrial irregularity and slightly but significantly reduced the incidence of ventricular fibrillation.
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PMID:The effect of bretylium on intracellular cardiac action potentials in relation to its anti-arrhythmic and local anaesthetic activity. 534 27

The exact relationship between cardiac arrhythmias and sudden infant death syndrome (SIDS) is uncertain. Several reports have implicated both ventricular and supraventricular arrhythmias in isolated cases, but there have been no studies of the incidence or type of arrhythmias that occur in populations at risk for SIDS. Of 1699 infants at high risk for SIDS, 60 (4%) were found to have a primary cardiac arrhythmia (i.e., not associated with disordered respiration or apnea). The incidence of atrial and ventricular premature beats, supraventricular tachycardia, and Wolff-Parkinson-White syndrome was similar to the incidence found in normal infants. Primary bradycardia (defined as a heart rate less than 60 for greater than 10 s not associated with abnormal respiration) was the most common arrhythmia, occurring with a frequency and severity not seen in normal infants. Thirty-two infants experienced periodic bradycardia. In 19 of these latter infants, there were symptoms associated with these bradyarrhythmias that necessitated treatment. Heart rates as low as 20 beats/min were recorded. One infant presented with an episode of ventricular fibrillation and on further evaluation was noted to have recurrent bradyarrhythmias. In no infant was there abnormal prolongation of the QT interval. Primary bradyarrhythmias are seen at an increased incidence in infants at high risk for SIDS and may play a causal role in this syndrome. Most symptomatic infants can be adequately controlled with sympathomimetic or parasympatholytic therapy. Other cardiac arrhythmias occur at a rate similar to that in normal infants and are therefore unlikely to play a major role in SIDS.
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PMID:Incidence and significance of primary abnormalities of cardiac rhythm in infants at high risk for sudden infant death syndrome. 608 2

Beta-adrenergic blocking agents differ considerably in their effects on myocardial excitable properties. The possibility that intrinsic sympathomimetic activity might contribute to such differences has not been adequately explored. This study examined the influence of intrinsic sympathomimetic activity on the electrophysiologic effects of three agents with varying degrees of such activity. Intravenous propranolol (0.5 mg/kg), oxprenolol (0.5 mg/kg) and pindolol (0.05 mg/kg) were administered in 16 anesthetized dogs. The effects of the drugs on ventricular vulnerability were studied over a 2 hour period. Propranolol and oxprenolol raised the ventricular fibrillation threshold by 42 and 56%, respectively. In contrast, pindolol resulted in an elevation of only 25%. After depletion of endogenous norepinephrine stores using reserpine, pindolol led to a decrease of the ventricular fibrillation threshold, which was reversed by propranolol. These data indicate that intrinsic sympathomimetic activity of beta-adrenergic blocking agents substantially alters their ultimate effect on myocardial excitable properties.
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PMID:Intrinsic sympathomimetic activity and the effects of beta-adrenergic blocking drugs on vulnerability to ventricular fibrillation. 613 90

The effects of several beta-adrenoceptor blocking agents, [+), (-) and (+/-)-oxprenolol, p-oxprenolol, practolol, propranolol and timolol) were investigated on the ventricular arrhythmias occurring within the first 30 min of acutely ligating the main left coronary artery in anaesthetized rats. The degree of cardiac and vascular beta-adrenoceptor blockade was also assessed. All the compounds exhibited antiarrhythmic activity under these conditions. The degree of cardiac beta-adrenoceptor blockade required for this protection was less for the cardioselective agents, p-oxprenolol and practolol, than for the non-selective beta-adrenoceptor blocking agents. A comparison of the two isomers of oxprenolol demonstrated that the (-)-isomer markedly suppressed ischaemic arrhythmias (ventricular ectopic beats, incidence and duration of ventricular tachycardia and duration of ventricular fibrillation) more effectively than the (+)-isomer. Compounds possessing intrinsic sympathomimetic activity (ISA) caused less marked haemodynamic changes (in equivalent beta-blocking doses) than those that did not possess this ancillary property. The membrane stabilizing activity of oxprenolol and p-oxprenolol did not appear to contribute to the antiarrhythmic activity of these agents; however, the membrane stabilizing activity of propranolol may contribute to its effectiveness. In all the drugs studied, the main pharmacological property required to suppress early postischaemic arrhythmias is blockade of cardiac beta-adrenoceptors.
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PMID:The effect of beta-adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats. 614 49

Experience with bretylium tosylate accumulated during a period of over 10 years, during which time greater than 1,500 patients with acute myocardial infarction were treated, is summarized. On the diagnosis of acute infarction, the agent was given by continuous intravenous drip at a rate of 10 mg/kg/24 hours for 5 to 7 days for prophylaxis of ventricular fibrillation. Bretylium administration prevented primary ventricular fibrillation in about 99% of these patients. No undesirable side effects were observed with this protocol, which lessens the initial sympathomimetic effect of the drug while allowing sufficient time for the adrenergic neuronal blocking effect to develop. The beneficial effects of the drug are believed to be due, in part, to a direct electrophysiologic effect on both normal and ischemic myocardium. This effect equalizes the duration of both the effective refractory periods and the ventricular action potentials, and it creates conditions capable of blocking reentrant pathways. Bretylium stabilizes the duration of electrical systole in patients with acute myocardial infarction. Hemodynamic studies during bretylium treatment further confirm the effectiveness of this drug and have prompted additional studies to evaluate its potential as an agent capable of decreasing impedance in acute myocardial infarction.
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PMID:Bretylium tosylate in patients with acute myocardial infarction. 646 96

The complications of myocardial infarction after transfer from the Coronary Care Unit on the 6th day were analysed bu a retrospective study of 3,460 computerised case reports (1973-1980). The mortality rate was 6% (1/3 of hospital deaths) in the period from the 7th day to discharge from hospital (14th to 30th day). Cardiac arrest as not uncommon (20% of all cardiac arrests) but the prognosis was better thn during the initial phase (p less than 0.05) as the mechanism was more commonly ventricular fibrillation or tachycardia (p less than 0.05). This series was compared with a similar population from 1970-1973; an improvement was observed in global hospital mortality (27% previously compared to 17%, in the study series, p less than 0.001). As the population were comparable, this phenomenon seems to be related to better treatment of shock and cardiac failure and the advances in cardiac surgery during the initial phase of infarction. Thd commonest mechanical complication was ventricular aneurysm; its occurrence does not influence the vital prognosis during this period. The incidence of cardiac arrest and death due to cardiac failure is not negligible after the first week of myocardial infarction. Therefore, we do not believe that the hospital period should be reduced after myocardial infarction. Special training of the nursing staff is essential for the successful treatment of these complications. The global prognosis could be improved by the rehabilitation of digitalis therapy and the introduction of new sympathomimetic amines in the acute phase of myocardial infarction.
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PMID:[Complications of myocardial infarction between the 2d and 4th week]. 681 81

It has become increasingly apparent that cocaine abuse can provoke lethal cardiac events, including myocardial infarction and ventricular fibrillation. The mechanisms responsible for these cardiotoxic actions of cocaine largely remain to be determined. Cocaine has two primary pharmacological properties that can adversely affect the heart and vasculature. Cocaine acts both as a local anesthetic (sodium and potassium channel blockade) and as a powerful cardiac stimulant that accentuates the actions of the sympathetic nervous system (inhibition of central and peripheral neuronal catecholamine uptake). The local anesthetic properties could impair impulse conduction, as well as elicit inhomogeneities in repolarization (refractory period), which creates an ideal substrate for reentrant arrhythmias. In addition, high doses of cocaine can depress contractile function due to inhibition of sodium/calcium exchange that results from decreased sodium influx (local anesthetic action). These actions are particularly obvious when sympathomimetic effects of cocaine are blunted. In a similar manner, the cocaine-induced accumulation of catecholamines potentiates the activation of alpha- and beta-adrenergic receptors, which can provoke coronary vasospasm (myocardial ischemia and infarction), increased contractile force (increased metabolic demand), and cardiac arrhythmias. The activation of adrenergic receptors will elicit a cascade of second messengers, ultimately provoking an increase in cytosolic calcium. These elevations in cytosolic calcium can provoke oscillations in membrane potential, triggering sustained action potential generation and extrasystoles. In particular, activation of the alpha IA-adrenergic receptor subtype and corresponding increase in calcium influx via voltage sensitive (L type) channels may play a critical role in the genesis of malignant arrhythmias. Thus, the adrenergic and local anesthetic properties of cocaine could act synergistically to elicit toxic actions on the heart.
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PMID:Cocaine: a review of its toxic actions on cardiac function. 761 73

This review provides a 20-year perspective on the most significant reports on antiarrhythmic drug therapy of ventricular arrhythmias, with particular reference to the CAST trials. The following conclusions are drawn: 1. Based on the CAST trials and other studies investigating the effectiveness of antiarrhythmic agents during the last 20 years, prophylactic treatment with antiarrhythmic class I, III and IV drugs after myocardial infarctions is not indicated. 2. Betablockers without intrinsic sympathomimetic activity are effective in the prevention of reinfarction and sudden cardiac death. 3. The effectiveness of amiodarone as secondary prophylaxis is currently under investigation in several multicenter trials. 4. Antiarrhythmic intervention is indicated in patients with hemodynamically compromising ventricular tachycardia or ventricular fibrillation, irrespective of spontaneous ventricular arrhythmias. Effective treatment with arrhythmic agents can be achieved in approximately half of the patients. Arrhythmia surgery, implantable cardioverters/defibrillators, or heart transplantation are possible alternative treatment modalities.
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PMID:[Anti-arrhythmia agents in the therapy of ventricular arrhythmias in the post-CAST era]. 793 21


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