Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial and coronary sinus catecholamine concentrations were measured during dynamic exercise in patients to assess the sympathetic response. Arterial concentrations increased from 1.77 nmol/1 (SEM = 0.53, n = 7) (control) to 2.95 nmol/1 (SEM = 0.65, n = 7) during exercise (0.05 greater than P greater than 0.01) and coronary sinus concentrations from 2.78 nmol/1 (SEM = 0.53, n = 7) (control) to 4.43 nmol/1 (SEM = 0.71, n = 7) (0.05 greater than P greater than 0.01). Resting, and exercise, arterial-coronary sinus differences in catecholamine concentrations were not statistically significant. In some patients, higher catecholamine concentrations occurred post-exercise than during exercise. The coronary sinus-arterial difference in catecholamine concentration during exercise was greatest in the one patient who developed angina pectoris. Cyclic-AMP concentrations were also measured, but these did not change significantly, consistent with the predominantly noradrenaline response to exercise.
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PMID:Arterial and coronary sinus catecholamines and cyclic-AMP during dynamic supine exercise in patients with chest pain. 20 94

The application of cyclic AMP as a marker of myocardial ischemia in humans with coronary artery disease has been investigated during pacing-induced angina. Cyclic AMP was determined by a radioimmunoassay. In 15 patients myocardial lactate extraction at rest (20 +/- 12%) converted to production levels (-30 +/- 23%) during angina (p less than 0.0005). Insignificant changes occurred in coronary venous plasma cyclic-AMP levels. The mean myocardial cyclic-AMP extraction at rest (0.3 +/- 8.7%) converted to small release values (-6.0 +/-11%) during angina (= n.s.). No significant correlation was found between myocardial lactate and cyclic-AMP uptake or release. Therefore, cyclic AMP is an insensitive marker in the evaluation of myocardial ischemia.
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PMID:Myocardial extraction of cyclic AMP during pacing-induced angina. 22 57

The blocking of the creatinphosphokinase by 1-fluoro-2,4-dinitrobenzene (FDNB) allows to investigate the relationship between ATP-supply, contractility and relaxability of the frog's myocardium. In isotonically working isolated ventricles of frogs the time of work, systolic and diastolic volume, velocity of contraction and relaxation as well as the levels of CP, ATP, ADP and AMP were measured at different intervals until termination of each experiment. CP shows a small variation, ATP decreases to 60% and ADP + AMP increase for the same amount under FDNB during the development of a slight inhibition of contractility and a continuously growing inhibition and retardation of relaxation until systolic arrest. ATP content and volume of relaxation correlated strictly. The contracture and the diminished contractility are caused by the decrease of ATP, producing a lack of substrate for Ca transport and actin-myosin-ATPase. This models the course of events during an insufficiency like in angina pectoris and in myocardial infarction.
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PMID:[Mechanical characteristics of isotonic work and high-energy phosphates in frog ventricle after 1-fluoro-2,4-dinitrobenzene]. 31 Jun 11

Calcium channel blockers (CCBs), which are used clinically for treatment of angina and hypertension, are known to inhibit calcium influx into arterial smooth muscle cells and thereby decrease smooth muscle cell contraction. In addition, they prevent cholesteryl ester (CE) accumulation, the hallmark of human atherosclerosis, in arteries of cholesterol-fed animals by cellular mechanisms that remain undefined. To assess whether CCBs enhance CE hydrolysis and reduce CE accumulation in human arterial cells, we measured activities of the CE metabolic cycle in aortic tissues that were stripped of endothelial cells and adventitia from 35 patients undergoing coronary artery bypass surgery. Patients who were treated with either nifedipine or diltiazem (n = 23) for several months demonstrated a threefold increase in arterial CE hydrolytic activities compared with untreated patients. This difference was independent of serum cholesterol levels, age, or treatment with other medications. No effects were observed on CE synthetic activity. Cyclic AMP levels in the aortic tissue of patients treated with CCBs were also significantly elevated twofold to threefold. In addition, both free and esterified cholesterol were significantly reduced in aortic tissue from patients taking CCBs compared with untreated patients. These data are the first to show that CCBs can increase CE hydrolysis in human aortic tissue by increasing intracellular cyclic AMP with resultant decrease in CE accumulation. Collectively, these findings support the hypothesis that CCBs can act as antiatherosclerotic agents in human tissue by mobilizing stored CE in the arterial wall.
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PMID:Calcium channel blockers enhance cholesteryl ester hydrolysis and decrease total cholesterol accumulation in human aortic tissue. 215 60

In a prospective study, platelet aggregation in platelet-rich plasma after ADP stimulation (0.5, 1.0 and 10 mumol/l) and collagen (1 and 5 micrograms/ml) was measured in 36 patients with coronary heart disease, 18 with angina at rest during the eight hours preceding the time of blood sampling, and 18 patients with stable, exercise-dependent angina, matched for age and sex. In addition, c-AMP was determined, before and (as a measure of platelet adenylate cyclase activity) after stimulation of this enzyme by prostaglandin E1 (10 mumol/l for 30 sec). There were no differences between all the tested ADP and collagen concentrations with regard to platelet aggregation. c-AMP levels were also similar. Thus, in patients with unstable angina there was no evidence for generalized hyperaggregation of platelets in comparison with control subjects who had stable exercise-dependent angina.
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PMID:[Thrombocyte function in unstable angina pectoris]. 284 Feb 54

Ten male patients suffering from stable angina pectoris were studied at rest and immediately after exercise during treatment either with timolol (a non-selective beta-blocker) or with metoprolol (a beta 1-selective blocker). Timolol induced a significant increase in platelet aggregation and a reduction in platelet cyclic AMP, and it also raised the plasma adrenaline at rest and during exercise as compared to the pre-treatment level. Metoprolol had none of these effects. Prior to medication and during metoprolol treatment, exercise led to an increase in the peripheral platelet count, whereas timolol was associated with a reduction of platelets during physical effort. Neither drug affected platelet thromboxane B2 at rest. During exercise, its level was not affected in the pre-treatment period or during metoprolol treatment but it was sharply increased by timolol therapy.
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PMID:Differential effects of timolol and metoprolol on platelet function at rest and during exercise. 289 94

The widespread use of beta-adrenoceptor antagonists against hypertension, angina pectoris and migraine or as a preventive treatment after myocardial infarction has encouraged us to investigate the effects of these drugs on platelet function. The aim of this study was to examine whether beta-blocking drugs interfere with platelet beta- adrenoceptors and whether this dependency is related to their selectivity for beta-adrenoceptor subtypes. Beta-adrenoceptor stimulation of human platelets with isoprenaline increased cyclic AMP (cAMP), which is known to inhibit platelet aggregation. Furthermore, our studies showed that cAMP formation in vitro was stimulated by non-selective and beta 2-selective agonists, but not by the predominant beta 1-agonist prenalterol. Isoprenaline- stimulated cAMP formation was blocked by the non- selective beta-adrenoceptor antagonists propranolol, timolol, and alprenolol, while the beta 1-selective antagonists atenolol and metoprolol had no influence on an isoprenaline-induced cAMP formation. Receptor binding studies using (3H)-dihydroalprenolol revealed an IC50 value for propranolol of 85 nM, while metoprolol only displaced the bound (3H)-dihydroalprenolol at far higher concentrations (IC50, 20 microM). We conclude that the human platelet beta-adrenoceptors are mainly of the beta 2- subtype and that beta-adrenoceptor antagonists, especially the non-selective antagonists interfere with platelet function assessed as platelet cAMP formation.
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PMID:Characterization of human platelet beta-adrenoceptors. 300 61

Reduced responsiveness of platelets to prostacyclin, reported in vitro in patients with coronary artery disease, has been thought to be a factor predisposing toward coronary thrombosis and vasospasm as a result of enhanced in vivo release of cyclic endoperoxides and thromboxane A2 by the platelets. In this study, specific binding of prostacyclin to intact platelets was determined in patients with coronary artery disease by direct binding studies using 9-3H-prostacyclin sodium salt. In addition, the inhibitory effect of prostacyclin on primary aggregation induced by adenosine diphosphate and cyclic adenosine monophosphate (cyclic AMP) accumulation stimulated by prostacyclin was examined. Twenty patients with angiographically documented coronary artery disease and stable angina, 8 patients with acute myocardial infarction, 14 healthy volunteers and 10 patients with normal angiograms were studied. In patients with stable angina, binding capacity and affinity of platelet prostacyclin binding sites and prostacyclin-induced cyclic AMP accumulation were not different from those of control subjects. In patients with acute myocardial infarction, however, binding capacity of platelet prostacyclin receptors was significantly reduced (0.69 +/- 0.45 versus 1.35 +/- 0.37 pmol/10(9) platelets, p = 0.001) and the postreceptor response, represented by platelet responsiveness to prostacyclin and prostacyclin-induced cyclic AMP synthesis, was impaired. Because all patients with myocardial infarction were receiving intravenous heparin and nitroglycerin, which might interfere with platelet prostacyclin binding, competition experiments were performed in vitro. Neither heparin (3 to 250 IU/ml) nor nitroglycerin (0.8 to 22 microM) displaced specifically bound 9-3H-prostacyclin. L-Epinephrine in concentrations up to 10 microM also exhibited no competition with specific platelet prostacyclin binding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet prostacyclin binding in coronary artery disease. 301 61

The effect of 12 weeks supplementation with fish oil on the number of anginal attacks and consumption of glyceryltrinitrate in 36 patients with stable angina pectoris was evaluated in a clinically controlled trial using a vegetable oil as placebo. Fish oil caused a decrease in frequency of angina, but was not significantly superior to placebo. However, due to the small sample size and a high spontaneous variation in number of anginal attacks, a risk of up to 50% of overlooking a 30% reduction in anginal attacks could be estimated. A significant inhibition of the epinephrine-induced platelet aggregation and a significant increase in intraplatelet cyclic AMP were induced by fish oil.
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PMID:Fish oil in angina pectoris. 310 45

Metabolic support for the heart has been an attractive concept since the pioneering work of Sodi-Pallares et al. four decades ago.* Recently, interest has increased in the use of over-the-counter supplements and naturally occurring nutriceuticals for enhancement of cardiac and skeletal muscle performance. These include amino acids such as creatine, L-carnitine, and L-arginine, as well as vitamins and cofactors such as alpha-tocopherol and coenzyme Q. Like these other molecules, D-ribose is a naturally occurring compound. It is the sugar moiety of ATP and has also received interest as a metabolic supplement for the heart. The general hypothesis is that under certain pathologic cardiac conditions, nucleotides (particularly ATP, ADP, and AMP) are degraded and lost from the heart. The heart's ability to resynthesize ATP is then limited by the supply of D-ribose, which is a necessary component of the adenine nucleotide structure. In support of this hypothesis, recent reports have used D-ribose to increase tolerance to myocardial ischemia. Its use in patients with stable coronary artery disease improves time to exercise-induced angina and electrocardiographic changes. In conjunction with thallium imaging or dobutamine stress echocardiography, D-ribose supplementation has been used to enhance detection of hibernating myocardium. In this article, we review the biochemical basis for using supplemental D-ribose as metabolic support for the heart and discuss the experimental evidence for its benefit.
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PMID:D-Ribose as a supplement for cardiac energy metabolism. 1115 Mar 94


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