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)

68 patients with CHD and stable angina pectoris class 1-2 in the presence of extrasystole were examined (spiro-bicycle ergometry, Holter ECG monitoring) before and after a course of general iodobromide baths (38 patients) or general fresh-water baths (30 patients). General iodobromide baths exerted marked antiarrhythmic effect in coronary heart disease with stable angina pectoris, the occurrence of ventricular, supraventricular extrasystoles reduced at least by half. Painful and silent myocardial ischemia decreased. Due to training effect of iodobromide balneotherapy muscular performance and coronary heart reserves improved.
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PMID:[The effect of iodobromide baths on the physical work capacity and extrasystole in patients with ischemic heart disease and stable stenocardia]. 871 98

In this study we compared different dietary constituents and their effect on the angina threshold. We compared carbohydrate-rich, fat-rich and balanced liquid diets on effort tolerance in 14 patients of mean (range) 61 (41-73) years of age with chronic stable angina. On four different occasions at least 1 week apart, patients had exercise treadmill tests after an overnight fast and then after a rest period of 1 h ingested one of three different approximately isocalorific (about 4000 kJ) liquid drinks of 600 ml consisting mainly of: fat, carbohydrate or a balanced meal with an equal volume of water as control. Meals were given in random order. Analysis of the mean (SD) differences in heart rate between fasting and the post-prandial state for the different meals revealed a significant increase between water and the other meals, fat (+4(6) beats.min-1 P < 0.002), balanced (+9(17) beats.min-1 P < 0.004), and carbohydrate (+10(12) beats.min-1 P < 0.0002). There was no significant difference between the groups as regards systolic or diastolic blood pressure. Cardiac output increased following the meals but decreased after water; however, there was a significant difference between water and balanced meals. Exercise tolerance fell following all the meals but was significantly greater after a balanced (mean (SD) -108(129) s P < 0.01) and carbohydrate meal (-92(52) s P < 0.001). The reduction in exercise duration following a fat meal (-36(53)s) was not significantly different from that following water (-8(43) s) but was significantly smaller than after a carbohydrate meal (P < 0.02). Time to 1 mm of ST depression showed similar changes to that of total exercise duration, being significantly lower after a carbohydrate (mean (SD) -76(77) s P < 0.01) and balanced meal (-76(63) s P < 0.005). Time to 1 mm ST depression, although reduced by a fat meal (-15(84) s) was significantly less than after a carbohydrate meal (P < 0.02). In conclusion, patients with chronic stable angina have impaired effort tolerance and a lower angina threshold after high calorie containing liquid meals. Meals rich in carbohydrate have greater effects than meals where the majority of calories are derived from fat. Patients should be advised to avoid exercise in the first 30 min after eating.
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PMID:The effect of meals of differing composition on exercise tolerance in patients with angina pectoris. 873 5

We have shown that unlike fat, protein, xylose, or water, the carbohydrate component of the meal accelerates myocardial ischemia, reduces exercise capacity, and is associated with a more rapid increase in the determinants of myocardial oxygen consumption than exercise in the fasting state. Our results suggest a role for a larger increase in sympathetic nervous activity and/or release of vasoactive gastrointestinal peptides after carbohydrate, but not fat or protein, meals in postprandial angina.
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PMID:Effects of components of meals (carbohydrate, fat, protein) in causing postprandial exertional angina pectoris. 916 67

1. The review summarizes the most important data known so far on chemistry, pharmacodynamics, toxicology and clinics of the investigational agent, pyridoindole stobadine. 2. Stobadine was shown to be able to scavenge hydroxyl, peroxyl and alkoxyl radicals, to quench singlet oxygen, to repair oxidized amino acids and to preserve oxidation of SH groups by one-electron donation. These effects originated from its ability to form a stable nitrogen-centered radical on indole nitrogen. Consequently, it was able to diminish lipid peroxidation and protein impairment under oxidative stress. 3. In various in vitro and in vivo animal models, stobadine was shown to diminish the impairment of the myocardium induced by mechanisms involving reactive oxygen species (e.g., myocardial infarction, hypoxia/ reoxygenation, catecholamine overexposure). 4. The neuroprotective effect of stobadine was demonstrated in a series of in vivo and in vitro models (brain in situ, brain slices, spinal cord, autonomic ganglia, etc.) during ischemia/reperfusion and hypoxia/ reoxygenation or in the presence of chemical systems generating free oxygen radicals, and so forth. Stobadine improved animal survival rate and synaptic transmission recovery, maintained SH tissue level and diminished lipid peroxidation as well as impairment of Ca-sequestering intracellular systems. 5. Oxidation of low-density lipoproteins (LDLs), which plays a major role in the development of atherosclerosis, was decreased by stobadine in vitro. Both lipid and protein (apo B) components of LDL were protected against Cu(2+)-induced oxidation by this agent. 6. Stobadine proved to be an effective protectant in models of free radical pathology in vivo, such as cyclophosphamide-, MNNG- or 60Co-induced mutagenesis and alloxan-induced hyperglycemia. 7. Besides other remarkable pharmacodynamic effects, stobadine exerts antidysrhythmic, local anesthetic, alpha-adrenolytic, antihistaminic, myorelaxant and antiulcerogenic actions. 8. Pharmacokinetic analyses demonstrated that stobadine was readily absorbed from the gastrointestinal tract. Thanks to its balanced lipo-hydrophilic properties, it was distributed over both water and lipid phases in biological tissues. It was shown to easily penetrate the blood-brain barrier. 9. Acute, subchronic and chronic toxicity studies in several animal species, as well as numerous analyses of embryotoxicity, teratogenicity, mutagenicity and genotoxicity, revealed only a negligible toxic potential of this agent. 10. Phase-one clinical study demonstrated safety of the compound. Only slight side effects--namely, a slight hypotension and a slight sedative effect--were observed subsequent to the highest dose used. In phase-two clinical study, the patients with angina pectoris treated for 4 weeks with stobadine showed a significant decrease in the frequency of anginal attacks, in the number of self-administrations of sublingual nitroglycerine and in plasma lipoprotein, cholesterol and triglyceride levels. A slight decrease in systolic and diastolic blood pressure also was observed. 11. It is suggested that stobadine may be considered a contribution to the search for new effective cardio- and neuroprotectants based on antioxidant or free radical scavenging mechanisms of action.
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PMID:Antioxidant and pharmacodynamic effects of pyridoindole stobadine. 955 11

When used as first-line treatment, any monotherapy selected from one of the main classes of agents for the management of slight to moderate arterial hypertension cannot be expected to have a success rate exceeding 60%. However, this level of efficacy approaches 80% if two classes of antihypertensive drugs with complementary modes of action are combined--a notable example being the combination of a beta-blocker, atenolol 50 mg, and a calcium antagonist, sustained-release nifedipine 20 mg. This fixed combination provides efficacy and tolerability in the treatment of arterial hypertension. Atenolol has beta-adrenolytic properties similar to those of propranolol, the most commonly named comparator drug. Atenolol is a selective beta 1-adrenergic antagonist with negative chronotropic, bathmotropic, dromotropic and inotropic actions. Because of its selectivity, it induces only moderate vasoconstriction. Its cardioselective nature diminishes the risk of bronchospasm, an event commonly induced by this type of drug. Atenolol reduces renin secretion from the renin-angiotensin system and consequently decreases the production of angiotensin II and plasma aldosterone. The renal effects of atenolol are an increase in both diuresis and natriuresis, with a reduction in the renal plasma flow. beta-Adrenergic antagonists in general modify carbohydrate metabolism and may mask the precursor signs of hypoglycaemia. They have a negligible effect upon lipid metabolism and practically no effect on total or high density lipoprotein cholesterol levels. Nifedipine belongs to the class of dihydropyridines. It acts by blocking the influx of calcium ions through the slow channels. Although a potent vasodilating agent, nifedipine does not induce tachycardia or water-sodium retention. The negative inotropic effect observed in vitro has not been reported in humans; the coronary dilatation produced by nifedipine is indisputable, both in unstable angina and exertional or exercise-induced angina. However, its cardioprotective effect remains questionable outside the context of recent-onset atheromatous plaques. Nifedipine increases renal blood flow and is practically devoid of diabetes-inducing factors. The fixed combination of atenolol 50 mg and sustained release nifedipine 20 mg offers a particularly interesting complementary action, the beta-blocker reducing the dihydropyridine-induced activation of the sympathetic nervous system and the latter reducing the vasoconstriction induced by the beta-blocker. Compared with each agent used alone, the pharmacokinetic profiles of atenolol and nifedipine remain unmodified by their administration in the fixed combination.
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PMID:[Pharmacologic importance of the combination atenolol/nifedipine in hypertensive patients]. 981 39

73 patients with ischemic heart disease (IHD) and stable angina pectoris of NYHA class I and II underwent balneotherapy. 43 of them took a course of sodium chloride baths, 30 control patients took common water baths. As shown by spiroveloergometry and Holter monitoring, sodium chloride baths are a good training modality in IHD patients. They enhance muscular performance and coronary heart reserve, reduce the mean 24-h number of ventricular extrasystoles by 49.9%, supraventricular extrasystoles by 57.5%.
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PMID:[The effect of sodium chloride baths on the physical work capacity and extrasystole of patients with ischemic heart disease and stable stenocardia]. 1042 66

Reactive oxygen species are thought to mediate reperfusion injury after rapid revascularization for acute myocardial infarction (AMI) and 8-epi prostaglandin (PG) F2alpha, a free-radical catalyzed product of arachidonic acid, has been proposed as an indicator of oxidative stress in vivo during myocardial reperfusion. The time course of urinary 8-epi PGF2alpha excretion after primary coronary angioplasty (PTCA) for AMI was investigated, as well as the effect of prior administration of vitamin C. Urine samples, 1 before and 5 after primary PTCA (0-30, 30-60, 60-90, 90-120 and 120-150 min), were collected in 11 patients with AMI undergoing primary PTCA (Group 1), 10 patients with AMI treated with water-soluble vitamin C at an initial dose of 2.0 g followed by a constant infusion at 20mg/min prior to primary PTCA (Group 2), and 6 patients with stable effort angina undergoing elective PTCA (Group 3). 8-epi PGF2alpha was measured by enzyme immunoassay. There were no significant differences in urinary 8-epi PGF2alpha excretion at baseline among the 3 groups. In Group 1, urinary 8-epi PGF2alpha excretion (ng/mmol creatinine) significantly increased from 60+/-8 at baseline to 122+/-16 at 60-90 min (p<0.001), and declined to the baseline level at 120-150 min after primary PTCA. In Group 2, it also increased from 72+/-12 to 123+/-15 at 60-90 min (p<0.01), and the percent increase did not differ from that in Group 1. In Group 3, it remained unchanged during the study period. The free radical production is rapidly and transiently enhanced after primary PTCA for AMI, and vitamin C fails to suppress it.
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PMID:Time course of free radical production after primary coronary angioplasty for acute myocardial infarction and the effect of vitamin C. 1061 35

Balneotherapy was given to 113 patients with ischemic heart disease (IHD) with stable angina (functional class I and II). 40 patients and 43 patients took radon baths (40 nCi/l and 120 nCi/l, respectively), 30 patients took the course of fresh-water baths. Treatment results were assessed at spiroveloergometry and ambulatory Holter monitoring. Radon baths had a training effect in IHD with extra-systole. It manifests in higher physical performance and coronary heart reserve. Antiarrhythmic effect of the radon baths was different: a significant reduction in the average number of 24-h ventricular extrasystoles by 78.1, supraventricular extrasystoles by 92.3%, and by 79.9 and 94.7% for the 40 nCi/l baths and 120 nCi/l baths, respectively.
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PMID:[The effect of radon baths on the physical work capacity and extrasystole in patients with ischemic heart disease and stable stenocardia]. 1064 38

The award of the Nobel Prize in Physiology and Medicine for 1998 bears witness to the 'explosive' field of nitric oxide (NO), and who would have thought the explosive nitroglycerin owed its therapeutic effectiveness to this little molecule? NO is also involved in causing penile erection, which has brought sildenafil to the aid of patients with erectile dysfunction. However, emerging evidence in animals and in vitro studies indicates that NO also inhibits steroidogenesis, which may have repercussions in humans. The decrease in androgen secretion may impact on secondary sexual characteristics, including penile size. The tolerance to the nitrate therapy in angina, characterized by volume expansion and not due to sodium retention, may also be related to steroid hormone deficiency. Decreased cortisol secretion may impair water excretion, resulting in volume expansion. Impaired aldosterone secretion would cause hyponatraemia with resultant raised renin. I hypothesize that continuous therapy with nitrates and sildenafil will result in diminished levels of steroid hormones with predicted sequelae.
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PMID:Is steroid deficiency the cause of tolerance in nitrate therapy? 1100 58

Nitrites and nitrates are consumed nonchalantly in diet. Organic nitrates are also used as vasodilators in angina pectoris, but the therapy is associated with tolerance whose mechanism remains elusive. Previously, we found inorganic nitrate inhibited steroidogenesis in vitro. Because adrenocorticoids regulate water and electrolyte metabolism, tolerance may ensue from steroid deficiency. We have studied the effects of nitrite and nitrate on in vitro synthesis and in vivo blood levels of steroid hormones. In vitro, nitrite was more potent than nitrate in inhibiting human chorionic gonadotropin (hCG)-stimulated androgen synthesis by Mouse Leydig Tumor cells. At concentrations above 42 mM, nitrite completely inhibited androgen synthesis, and, unlike nitrate, the inhibition was irreversible by increasing hCG concentration. The cAMP production remained intact but reduced with both ions. The nitric oxide (NO) scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxy-3-oxide (c-PTIO) significantly increased hCG- or cAMP-stimulated androgen synthesis in all buffers, suggesting that NO is a chemical species directly involved in the nitrite/nitrate-induced inhibition. This is further supported by c-PTIO countering the inhibitory action of methylene blue on androgen synthesis. Rats given distilled water containing 50 mg/L NaNO(2) or NaNO(3) for 4 weeks drank significantly less daily. At the end, their blood corticosterone and testosterone levels were significantly decreased. The adrenocortical histology showed bigger lipid droplets, which are pathogonomic of impaired steroidogenesis. Nitrite and nitrate are metabolized to NO, which binds heme in cytochrome P450 enzymes, thereby inhibiting steroidogenesis. Therapeutic nitrates likewise may decrease adrenal (and gonadal) steroidogenesis. Cortisol deficiency would impair water excretion causing volume expansion, and aldosterone deficiency would cause sodium loss and raised renin. Paradoxically, volume expansion without sodium retention and raised renin has all been reported in tolerance.
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PMID:Decreased steroid hormone synthesis from inorganic nitrite and nitrate: studies in vitro and in vivo. 1113 44


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