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)

Adrenaline, noradrenaline and dopamine excretion was investigated in essential hypertension (n = 20), atherosclerotic heart failure (n = 20, NYHA class II and III), chronic angina (n = 10) and in healthy controls, in four time intervals: between 600-1200, 1200-1800, 1800-2400, 2400-600. Fluorimetric method of Anton and Sayre was employed. In patients with essential hypertension the circadian rhythm of adrenaline, noradrenaline and dopamine excretion was maintained but in all time intervals excretion of dopamine was decreased. In individuals with congestive heart failure due to atherosclerosis and in patients with ischemic heart disease, physiological circadian rhythm of adrenaline and noradrenaline excretion was found to be abolished. This was not the case with dopamine excretion which was undisturbed.
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PMID:[Hypertension, heart failure and angina pectoris. Diurnal rhythm of urinary excretion of catecholamines]. 164 Jun 65

The clinical and haemodynamic effects of adrenaline infusion (30 ng kg-1 min-1) producing plasma adrenaline concentrations in the range seen during acute myocardial infarction and of placebo were investigated in a crossover design in 14 patients with stable coronary heart disease. Adrenaline infusion resulted in electrocardiographic evidence of myocardial ischaemia (greater than or equal to 1 mm (0.1 mV) horizontal or downsloping ST segment depression) in 10 patients and angina in four, although the mean (SEM) increase in heart rate was modest (14 (2) beats/min) and mean coronary vascular resistance fell from 1.56 (0.21) to 1.16 (0.14) mm Hg min ml-1 (p less than 0.005). New or increasingly frequent or complex ventricular arrhythmias occurred in five patients. Placebo infusion had no effect on the variables measured. Supine bicycle exercise during infusion of the saline placebo was associated with a similar degree of ST segment depression (0.9 (0.2) mm) as adrenaline infusion at rest (0.9 (0.1) mm) but exercise performed during adrenaline infusion (10 patients) resulted in more pronounced ST segment depression (1.9 (0.3) mm) (p less than 0.005) than either intervention alone. Angina occurred in three of 11 patients during control exercise and in six of 10 during the combination of adrenaline infusion and exercise. Such potentially adverse consequences of low dose adrenaline infusion in patients with stable coronary heart disease are consistent with the suggestion that adrenal activation is detrimental during acute myocardial infarction, being both arrhythmogenic and proischaemic.
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PMID:Myocardial ischaemia and ventricular arrhythmias precipitated by physiological concentrations of adrenaline in patients with coronary heart disease. 138 26

To identify the effect of myocardial ischemia on systemic neurohormones and vascular resistance, 32 untreated, normotensive patients with coronary artery disease underwent incremental atrial pacing until angina. Arterial and coronary venous lactate and arterial values of catecholamines and angiotensin II were determined at control, at maximal pacing rates, and at 1, 2, 5 and 30 minutes after pacing. Based on pacing-induced ST-segment depression (greater than or equal to 0.1 mV) or myocardial lactate production, or both, patients were selected as ischemic (n = 25) or nonischemic (n = 7). Baseline clinical and hemodynamic data were comparable. During pacing, chest pain was similar (20 ischemic vs 7 nonischemic patients). Also, hemodynamic measurements were comparable, except for contractility, which did not improve, and left ventricular end-diastolic pressure, which significantly increased in ischemic patients. Moreover, during ischemia arterial pressures increased significantly (13%) and systemic resistance increased from 1,470 +/- 60 (control) to 1,632 +/- 76 dynes.s.cm-5 5 minutes after pacing (p less than 0.05) in ischemic but not in nonischemic patients. Pacing did not affect neurohormones in nonischemic patients. In contrast, norepinephrine in ischemic patients increased significantly from 1.7 +/- 0.2 (control) to 2.6 +/- 0.3 (maximal pacing) and to 3.0 +/- 0.4 nmol/liter (1 minute after pacing), whereas angiotensin II levels increased from 6.2 +/- 1.4 (control) to 9.3 +/- 2.1 pmol/liter (1 minute after pacing, p less than 0.05). Epinephrine only increased during maximal rates (0.9 +/- 0.1 vs 0.6 +/- 0.1 nmol/liter at control, p less than 0.05). Thus, myocardial ischemia activates circulating catecholamines and angiotensin II, accompanied by systemic vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic neurohumoral activation and vasoconstriction during pacing-induced acute myocardial ischemia in patients with stable angina pectoris. 206 79

A study was made of the mechanisms mediating autonomic changes resulting from stimulation of a site in the lateral hypothalamic area (LHA). This site, when stimulated, induced angina-like ECG disturbances similar to those observed in some cases of brain traumas. These ECG changes were often associated with other autonomic changes, such as pressor response, tachycardia (in some cases bradycardia), nictitating membrane (NM) contraction and pupillary dilatation. Most symptoms were sympathetic: they were largely abolished by spinal cord section between C1 and C2, but were not affected by vagotomy, except that bradycardia was converted to tachycardia. Adrenal catecholamines were not involved since adrenal vein ligation was without effect. Hexamethonium (5-10 mg/kg) prevented pressor response and tachycardia in most cats but only partly protected against ECG changes and NM contractions. Atropine methyl nitrate (0.2 mg/kg) abolished the remaining ECG abnormalities and NM tension. The beta-receptor antagonists, propranolol and practolol (50 micrograms/kg) completely prevented the ECG changes induced either by isoprenaline or LHA stimulation. It is concluded that the symptoms induced by LHA stimulation result from noradrenaline release in the target organs.
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PMID:A pharmacological analysis of autonomic pathways mediating myocardial disturbances originating in a lateral hypothalamic area of the cat. 630 72

Patients suffering from stress-induced angina pectoris subjected to exertion show a decreased level of non-protein SH-groups in blood plasma and erythrocytes which depends on the level of myocardial hypoxia and may indicate metabolic exhaustion of the organism. Lowered concentrations of non-protein SH-groups are not a result of lipid peroxidation. Adrenalin is known to antagonize the depletion of non-protein SH-groups under exertion, while noradrenaline promotes the process of their oxidation. When the level of non-protein SH-groups decreases under exertion, the content of atherogenic lipids in blood does not increase, which implies that SH-groups are involved into the mechanism of appearance of atherogenic lipids in blood under exertion.
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PMID:[Non-protein sulfhydryl groups in the blood of patients with stenocardia induced by physical stress]. 775 64

Eight female patients (aged 51 to 65 years) with New York Heart Association class II angina pectoris, normal coronary angiograms, normal hyperventilation, and abnormal exercise stress tests (chest pain and ST depression), and 5 sex- and age-matched controls participated in this study. Epinephrine was given intravenously to both patients and controls at 5-minute intervals in doses of 0.1, 0.2, 0.3, 0.4, and 0.6 nmol/kg/min. After rest (15 minutes), the alpha-adrenoceptor antagonist phentolamine or placebo was administered intravenously to patients in a double-blind, crossover study on 2 separate occasions in doses of 250 micrograms/min for 5 minutes and 500 micrograms/min for the next 10 minutes; the epinephrine infusion was repeated. Blood pressure, heart rate, and electrocardiogram were monitored continuously and pain was estimated on the Borg CR-10 scale. On a third occasion, chest pain was induced in patients using the same epinephrine protocol during echocardiographic monitoring. In the control group, all patients received the maximal epinephrine dose. No chest discomfort or pain developed. In the patient group, the maximal tolerable epinephrine dose (0.39 +/- 0.19 nmol/kg/min) decreased diastolic pressure (-14 +/- 9 mm Hg, p < 0.01) and increased heart rate (+24 +/- 10 beats/min, p < 0.01), not statistically different from the control group. Pulse pressure increased in the patient group (27 +/- 17 mm Hg, p < 0.01) but not in the controls. Left ventricular ejection fraction at baseline was within reference limits (58% to 75%) and did not change during epinephrine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of epinephrine infusion on chest pain in syndrome X in the absence of signs of myocardial ischemia. 757 75

Abnormal constriction of coronary resistive vessels can induce angina and myocardial ischemia. The possibility that a microvascular vasomotor dysfunction could cause ischemia is in contrast with the well-known traditional notion that a metabolically induced vasodilation could compensate for the effect of an epicardial coronary stenosis. Vasoconstrictor stimuli can plausibly act on vessels situated immediately proximal (prearterioles) to those that can be dilated by ischemia metabolites (arterioles). This functional 2-compartment model of resistive vessels is based on the ability of different substances to cause opposite actions on resistive vessels with different sizes. The possible mechanisms of prearteriolar dysfunction, observed in patients with syndrome X, single vessel disease after a successful PTCA and in a subset of chronic stable patients include: an organic reduction of total vascular section; vascular smooth muscle hyperreactivity to heterogeneous constrictor stimuli; an impaired flow-mediated endothelium-dependent vasodilation (possibly due to a reduced NO and/or EDHF synthesis). The first and third hypothesis can only account for anginal episodes at effort while the second model could explain episodes occurring at rest and without an increase in heart rate. Those mechanisms causing an imbalance between myocardial oxygen supply and demand, induce an increased release of adenosine in order to promote a compensating vasodilation. Adenosine can possibly avoid the occurrence of ischemia but, being a powerful algogenic stimulus, causes pain. It is worth noting that the presence of patchy prearteriolar dysfunction induces areas with excessive release of adenosine. Since total vascular section is extremely large a massive adenosine spill-over can occur with a consequential boosting of algogenic and vasodilatory effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanisms of coronary microvascular dysfunction]. 802 13

1. The impact of oral acetylsalicylic acid treatment on the enhancing effect of adrenaline on platelet aggregation in vitro was investigated in patients with stable angina pectoris. In addition, the influence of different anticoagulants (i.e. hirudin and citrate) on platelet aggregation in vitro was compared. 2. Eighty-four patients with stable angina pectoris were studied. Sixteen patients were on acetylsalicylic acid treatment (150-250 mg daily), whereas 68 patients were free from acetylsalicylic acid. Platelet-rich-plasma was prepared from citrate- or hirudin-anticoagulated blood. The EC50 (i.e. the concentration of agonist required to produce half-maximal aggregation) for the ADP-induced extent of aggregation was determined. Thereafter the enhancing effect of adrenaline (10 and 50 nmol/l) on ADP-induced aggregation (at EC50) was investigated. 3. In the patients with angina, acetylsalicylic acid caused the expected effects on ADP-induced platelet responses. Adrenaline significantly enhanced both the extent of aggregation and the initial rate of aggregation (primary aggregation), irrespective of the anticoagulant used. In acetylsalicylic acid-treated patients (citrated platelet-rich plasma) the extent of aggregation was partly inhibited, but no significant effect on the rate of aggregation could be observed. 4. A comparative substudy of the anticoagulants in healthy subjects (n = 8) showed that both the aggregating effect of ADP per se and the enhancing effect of adrenaline on ADP-induced aggregation (at EC50) were less influenced by acetylsalicylic acid when evaluated in hirudinized platelet-rich plasma (i.e. with physiological levels of extracellular calcium) as compared with citrated platelet-rich plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of treatment with acetylsalicylic acid on the proaggregatory effects of adrenaline in vitro in patients with stable angina pectoris: influence of the anticoagulant. 828 46

Adrenalin is the drug for anaphylactic shock. The product is usable directly by the patient in the form of an auto-injectable kit, by the physician who treats by the sublingual or subcutaneous routes, in a resuscitation unit extra and inter-hospital by the intra-veinous route with cardiac monitoring. Precaution have to be observed (in angina especially), but it is without formal contra-indications. The beta 2 adrenergics are non-specific bronchodilators. Two categories are available: short action molecules, crisis drugs, prolonged activity molecules (greater than 12 hours). Several routes of administration are useable: spray or powder (inhalation) sub-cutaneous, taking by mouth.
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PMID:[Adrenaline and beta 2 adrenergics]. 1037 Jul 25

Platelet aggregation is an important in vitro test to assess platelet aggregation response in IHD. The present prospective case control study was undertaken to evaluate the platelet aggregation response in IHD and the effects of aspirin therapy on it. Platelet aggregation was conducted on whole blood by the Chrono- Log whole blood Aggrometer model 540-VS. Various agonists used for platelet aggregation were collagen, ADP, Epinephrine and Thrombin. High platelet aggregation was observed in-patients of IHD as compared to controls by few or all of the reagents used. Platelet aggregation was high in both MI and angina as compared to control cases. However, cases of MI showed higher response than those of angina. Aspirin intake was associated with a decrease in platelet aggregation in patients of IHD. The platelet aggregation response was higher in PRP as compared to whole blood with similar concentration of reagents, however whole blood was equally effective as PRP in detecting hyper-responsive platelets in--patients of IHD.
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PMID:Platelet aggregometric study on whole blood of patients with ischaemic heart disease. 1640 37


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