Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several large-scale, multicenter trials have been conducted to evaluate the effects of currently available calcium channel blockers on a variety of cardiac end points in patients with myocardial infarction. Results indicate that careful subgroup stratification is necessary if morbidity and mortality are to be favorably altered. Certain groups of patients who are at high risk of recurrent myocardial infarction (MI) or death must be targeted for more aggressive diagnosis and therapy. Subset analysis of the Multicenter Diltiazem Postinfarction Trial (MDPIT) provides detailed information about diltiazem's long-term benefit following non-Q-wave or inferior Q-wave MI, and its lack of efficacy in patients with extensive or prior MI. Concerning use of beta-blockers versus calcium channel blockers as secondary prevention following acute MI, the pathogenesis, clinical course, prognosis, anatomy, and histology of non-Q-wave MI differs appreciably from Q-wave MI, and hence it is logical to assume that secondary prophylaxis post-MI should differ for non-Q-wave versus Q-wave MI. It would appear that beta-blockers (particularly those agents without intrinsic sympathomimetic activity) are best suited for secondary prevention after Q-wave MI, whereas diltiazem is the only therapy of proven benefit for use after non-Q-wave MI.
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PMID:Management of non-Q-wave myocardial infarction: role of diltiazem versus beta-blocker therapy. 170 17

More and more patients with coronary heart disease (CAD) are admitted to intensive care units. The drugs used to treat these patients have various effects on the myocardium which must be known in order to avoid worsening the CAD. This review examines the metabolic effects on the myocardium of the most commonly used drugs in intensive care. The physiology of myocardial oxygen supply is first recalled with regard to the coronary circulation, myocardial oxygen extraction and consumption. Digitalis glycosides do not affect the coronary circulation, but the decrease myocardial oxygen consumption in patients with heart failure, mainly by lowering heart rate. Dihydropyridine calcium blockers (nifedipine, nicardipine) increase coronary blood flow, despite a decrease in arterial blood pressure. Their effects on myocardial oxygen consumption are mediated by a sympathetic reflex. Verapamil decreases the heart rate and myocardial inotropism, and is responsible for coronary vasodilation. The result is a decrease in myocardial oxygen consumption. Diltiazem and bepridil have almost similar effects: they decrease myocardial oxygen consumption and increase blood supply to the heart. It has been recently shown that verapamil was the most depressant calcium channel blocking agent, and that it resulted in the most important decrease in myocardial metabolism. Beta-blocking agents decrease myocardial metabolism, except those with an important intrinsic sympathomimetic activity, such as pindolol. Amiodarone can be considered as an alpha and beta blocking drug: its main effect is to counteract the effects of endogenous catecholamines on myocardial metabolism. The sympathomimetic amines (noradrenaline, adrenaline, isoprenaline, dopamine, dobutamine) increase, to different extents, myocardial oxygen consumption. Vasodilators, such as the nitrates or sodium nitroprusside, decrease cardiac filling pressures, and increase myocardial blood flow, thus lowering myocardial oxygen consumption. Phosphodiesterase inhibitors (amrinone, enoximone) have both an inotropic and a vasodilating effect. They decrease cardiac afterload, and increase blood supply to the myocardium; this compensates for the increase in myocardial oxygen consumption due to the increase in myocardial contractility. Because all the drugs used in intensive care have different effects on myocardial metabolism, their reasoned use should avoid an inappropriate increase in oxygen demand.
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PMID:[Changes in myocardial metabolism induced by drugs used during intensive care]. 197 Apr 63

Experiments were designed to investigate the effect of two calcium antagonists, diltiazem and nicardipine (concentration range: 10(-7)-10(-4) M), on the contractile responses to transmural nerve stimulation, exogenous noradrenaline and tyramine in isolated canine saphenous vein rings. Both diltiazem and nicardipine inhibited the contractile response to transmural nerve stimulation in a non-competitive, concentration-dependent manner. At a concentration of 10(-4) M, diltiazem and nicardipine inhibited the maximum contractile response to transmural nerve stimulation to 0.8 +/- 0.8% and 20 +/- 10% of control respectively. Effects of diltiazem and nicardipine (up to 10(-4)M) on the contractile response to exogenous noradrenaline were minimal. The only significant difference observed was a 30% depression of the maximum contractile response with a shift in ED50 at high concentrations of nicardipine. Diltiazem (up to 10(-4) M) had no significant effect on concentration-effect curves for tyramine. Nicardipine inhibited the response to tyramine in a non-competitive manner with the maximum response depressed to 46% of control at 10(-4) M-nicardipine. Release of [3H]noradrenaline during transmural nerve stimulation was reduced by both calcium antagonists in a concentration-dependent manner. However, release of [3H]noradrenaline produced by the indirect sympathomimetic agent tyramine was not significantly inhibited by nicardipine. These experiments suggest that the calcium antagonists diltiazem and nicardipine inhibit the contractile response to transmural nerve stimulation in the canine saphenous vein predominantly by inhibiting the release of endogenous noradrenaline. However, nicardipine appears to have an additional post-synaptic inhibitory effect on the responses to exogenous as well as endogenous noradrenaline.
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PMID:Effect of calcium antagonists on adrenergic mechanisms in canine saphenous veins. 372 10

Coronary arterial spasm plays an important role iun the production not only of variant angina but, also, of resting angina other than variant angina, of some exertional angina, and of some acute myocardial infarction. Coronary arterial spasm is most likely to occur at rest, particularly from midnight to early morning, and is usually not provoked by exercise in the daytime. This is related to the fact that the tone of coronary artery is increased from midnight to early morning, whereas it is decreased in the daytime after physical activities. Coronary arterial spasm can be induced by exercise, cold pressor test, hyperventilation, Valsalva maneuver, and the administration of pharmacological agents such as sympathomimetic agents (epinephrine, norepinephrine, etc.), beta-blocking agents (propranolol, etc.), parasympathomimetic agents (methacholine, pilocarpine, etc.), ergot alkaloids (ergonovine, ergotamine, etc.), alcohol, and others, particularly in the morning when spontaneous coronary arterial spasm is most likely to occur. Diltiazem and nifedipine, calcium-blocking agents, prevent coronary arterial spasm induced by these procedures in almost all patients. Phentolamine, an alpha-blocking agent, also suppresses coronary arterial spasm induced by these procedures in 81% of the patients. On the other hand, propranolol, a beta-blocking agent, is not only ineffective in suppressing coronary arterial spasm in 82% of the patients, but aggravates coronary arterial spasm in 41% of the patients. The acute attack of coronary arterial spasm can be promptly relieved by the administration of nitroglycerin.
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PMID:Coronary arterial spasm in ischemic heart disease and its pathogenesis. A review. 633 4