Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted in anesthetized dogs comparing the effects of PGA1, PGE2, and diazoxide on myocardial contractile force (MC). The three agents were given in successive bolus injections intravenously in equidepressor doses and myocardial contractile force was measured by means of a strain-gauge arch sutured onto the right ventricle. The drugs were administered before and during ganglionic (hexamethonium) and beta-blockade (practolol). Both PGA1, and PGE2 caused a marked rise in MC, 24 and 20 per cent, respectively, before blockade and 10 and 11 per cent during blockade. Diazoxide caused only a minimal rise, 0.9 per cent, before blockade and a marked fall, 27 per cent, during blockade. Diazoxide administration during left ventricular bypass indicates that the decrease in MC is not a direct result of alterations in preload or after load. It is suggested that hypertensive patients treated with autonomic blocking agents may be more susceptible to heart failure in response to diazoxide therapy.
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PMID:Effect of PGA1, PGE2, diazoxide on myocardial contractile force. 0 54

Dopamine is a direct-acting catecholamine with a short half-life that has many advantages in treating visceral hypoperfusion states such as shock and refractory heart failure. Unlike other inotropic drugs, dopamine directly dilates the mesenteric, renal, and cerebral vessels and redirects blood flow to essential viscera. This dopaminergic effect is prominent with doses of 100-700 mug/min in adults and is attenuated by phenothiazines and haloperidol. At doses of 700-1400 mug/min, dopamine also has a significant beta-adrenergic, inotropic effect, increasing myocardial contractility. The inotropic effect is equivalent to that of isoproterenol, epinephrine, and norepinephrine, but tachycardia, tachyarrhythmias, and angina may be less frequent with dopamine. In doses greater than 1400 mug/min, dopamine is a vasoconstrictor with pressor effects usually equivalent to that of norepinephrine. Dopamine dilates pupils, does not dilate bronchi, and does not shunt blood from viscera to skeletal muscles as does isoproterenol. Because dopamine increases myocardial contractility, selectively redistributes perfusion to essential viscera and allows a pharmacologic titration of effect, it is a logical first-choice catecholamine for treatment of shock and refractory heart failure.
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PMID:The clinical use of dopamine in the treatment of shock. 0 63

The effects of the cardioselective beta-blocker, metoprolol, were evaluated under double-blind conditions in eighteen patients with angina pectoris. During an introductory run-in period of eight weeks, a placebo was given single-blindly. Thereafter two double-blind crossover periods each of four weeks followed, either 20 mg metroprolol or placebo being given t.i.d. Metoprolol gave a significant reduction in the number of anginal attacks and in nitroglycerin consumption. The patients' subjective assessments of their daily angina pectoris symptoms also showed a significant improvement compared with the placebo. At the end of each period, a standardized exercise test was performed. In comparison with placebo, metoprolol gave a significant increase of total work performed until the appearance of 1 mm ST-segment depression and until the end of exercise. The heart rate was significantly reduced at rest and during exercise. The blood pressure was significantly reduced only during exercise. None of the patients reported any severe unwanted effects. The complaints reported were mild to moderate, and the frequency during metoprolol treatment was even lower than during placebo treatment. No signs or symptoms of cardiac failure were seen in any of these patients on any occasion. It is concluded that 20 mg metoprolol t.i.d. is of benefit in the treatment of angina pectoris but further benefit might be obtained with higher doses.
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PMID:Effects of the cardioselective beta-blocker metoprolol in angina pectoris. A subacute study with exercise tests. 0 92

The study of fluid and electrolyte disturbances by isotope radiodilution method is carried out in 22 patients with chronic respiratory insufficiency and cardiac failure. The simultaneous measurements of hydro-ionic compartments have been carried out with tritiated water (HTO), labelled sodium (22Na), labelled potassium (42K) and labelled bromine (82Br). From these measurements, the various water spaces are calculated: total water (ET) and extracellular fluids (LEC), also exchangeable electrolytes: sodium (NaE), potassium (KE), chlorine (ClE) and derived values. Results are compared to corresponding values in controls with the same obesity index. Patients with respiratory insufficiency show a fluid and sodium rise, similar to that found in cardiac failure and denutrition. The (NaE + KE)/ET ratio is not significantly decreased and the natremia is only slightly lower. There is no real potassium depletion in most patients.
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PMID:[Isotopic study of fluid and electrolyte disturbances in decompensated chronic respiratory insufficiency (author's transl)]. 0 42

The isolated perfused working rat heart preparation has been used to study the effects of respiratory acidosis on myocardial metabolism and contractilly. Hearts were perfused with 5 mM glucose and 10(-2) U/ml of insulin in order to enhance metabolsim of glucose relative to that of fatty acids. After perfusion with Krebs bicarbonate medium at pH 6.6, hearts rapidly ceased performing external work and peak left ventricular pressure fell by 75% after 5 minutes. Oxygen consumption, rate of ATP generation and overall glycolytic flux also declined rapidly. After about 2 minutes of perfusion, the fall of glycolytic flux showed a partial reversal, which was largely accounted for by increased lactate production, so that glucose oxidation decreased further. The reversal of glycoltic flux could be accounted for by partial release of H+ inhibition of phospho-fructokinase by increased tissue levels of adenosine 5'-diphosphate (ADP), adenosine monophosphate (AMP) and P1 and decreased levels of adenosine triphosphate (ATP) and creatine phosphate. The increased proportion of glucose uptake converted to lactate together with an increase of the tissue lactate/pyruvate ratio could be accounted for by inhibition of the malate-aspartate cycle combined with tissue hypoxia. Lactate accumulated in the tissue as a result of a decreased permeability of the plasma membrane to lactate. Decreased oxygen delivery to the myocardium was caused by secondary constriction of the coronary vessels. In further experiments, the coronary flow was regulated by an external pump which delivered fluid at a controlled rate into the aortic cannula above the coronary arteries, and the degree of tissue hypoxia was monitored by measuring changes of pyridine nucleotide reduction state by surface fluorescence techniques. The effects of acidosis uncomplicated by possible hypoxia were compared directly with those produced by ischemic hypoxia. The effects of acidosis under these conditions were similar to those described above, and to those produced by ischemia. From these and other data it is concluded that the effects of ischemia are caused by a lowering of the intracellular pH, which decreases the rate of energy production relative to the rate of energy demand. However, it is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart. Possible causes of irreversible heart failure after prolonged ischemia are discussed.
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PMID:Contribution of tissue acidosis to ischemic injury in the perfused rat heart. 0 93

The interaction between cedilanid-D and metoprolol, a selective beta receptor blocking agent, on exercise tolerance and systolic intervals was studied in 15 patients with angina pectoris. The patients had been treated with metoprolol for several months in a dose of 50 mg, three times daily (one patient received 25 mg three times daily). Each patient participated in two studies separated by at least 1 week. After arriving at the laboratory each received 50 mg of metoprolol orally; thereafter, either cedilanid-D or placebo was infused intravenously in a double-blind study performed in randomized order. When the effect of the drugs was maximal, the systolic intervals and the heart volume were recorded at rest, and the exercise tolerance was tested with a bicycle ergometer. The mean maximal value of plasma concentrations of metoprolol assessed during the study was about 50 ng/ml but the variation among subjects was great (20 to 187 ng/ml). After administration of cedilanid-D there was a shortening of the pre-ejection period and left ventricular ejection time compared with results after placebo; the reduction was similar to that found after administration of cedilanid-D without beta blocking drugs. The total heart volume decreased by an average of 55 ml, but the individual variation was great. The patients' average work capacity, expressed as total work, was not altered by cedilanid-D when compared with results after placebo. No relation was found between initial heart size and the effect of cedilanid-D on capacity for physical work. It therefore appears that there is no indication for the routine use of digitalis during beta blocking therapy in patients with angina pectoris who do not have cardiac failure.
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PMID:Effects of cedilanid-D in combination with metoprolol on exercise tolerance and systolic time intervals in angina pectoris. 0 61

The effect of a cardioselective beta-adrenergic blocking agent, metoprolol, on symptoms and exercise tolerance was studied in 16 patients with angina pectoris. Metroprolol was compared with placebo at two dose levels (20 mg t.d.s. and 50 mg t.d.s.) in a double-blind trial in 14 patients. Compared with placebo, metroprolol caused a significant reduction of heart rate and systolic blood pressure during exercise, and consequently a reduction of the rate-pressure product. The reduction was greater with 50 mg t.d.s. than with 20 mg t.d.s. The exercise tolerance measured as total work increased significantly by 21 per cent during treatment with metroprolol 20 mg t.d.s., and by 17 per cent during treatment with 50 mg t.d.s. There was a reduction in the number of anginal attacks and in nitroglycerin consumption, and subjective improvement of angina pectoris at both dose levels of metroprolol. No signs of cardiac failure appeared during any of the four treatment periods. Heart volume showed no significant change. Unwanted effects were of the same frequency and severity during treatment with metroprolol at both dose levels as with placebo.
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PMID:Effects of the cardioselective beta-adrenergic receptor blocking agent metoprolol in angina pectoris. Subacute study with exercise tests. 0 80

When rat hearts were subjected to abrupt hypoxia the onset of NADH changes as measured by epicardial fluorescence and of depressed contractility occurred at similar times. Direct measurements of changes in tissue metabolism lagged behind changes in fluorescence and contractility. Calculated NAD:NADH ratios became reduced more rapidly and to a greater extent in the cytoplasm than in the mitochondria, but did not necessarily signal greater changes in total NADH. The detection of depressed contractility before a fall in intracellular pH or a rise in intracellular lactate casts doubt on the postulate that an increase in hydrogen ion is the primary cause of hypoxic myocardial failure.
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PMID:Early changes in myocardial hypoxia: relations among mechanical function, pH, and intracellular redox states. 0 55

Eighteen patients with angina pectoris, who had previously participated in a cross-over study with 20 mg metoprolol t.i.d. and placebo, have been included in this study. During an introductory six-month open tolerability study, all patients were treated with 50 mg metoprolol t.i.d. and during a subsequent cross-over study, the efficacy of this dose was compared with that of placebo under double-blind conditions. An exercise was performed at the end of each cross-over period. Metoprolol, in a dose of 50 mg t.i.d., gave a significant improvement compared with placebo in respect of the number of anginal attacks, nitroglycerin consumption and daily subjective assessment of the patients' anginal symptoms. Metoprolol also gave a significant increase in exercise capacity, both until the appearance of 1 mm ST segment depression and until the end of exercise. Heart rate and blood pressure were reduced both at rest and during exercise. No severe unwanted effects were observed during this study ranging over eight months, and none of the patients had any signs or symptoms of cardiac failure or pulmonary dysfunction on any occasion. Unwanted effects reported were mild to moderate, and the frequency was the same as during placebo treatment. No abnormal laboratory findings were observed and the relative heart volume was not significantly changed. Administration of 50 mg metoprolol t.i.d. seems to be of greater benefit than 20 mg metoprolol t.i.d., previously investigated in these patients.
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PMID:Effects of metoprolol in angina pectoris. A subacute study with exercise tests and a long-term tolerability study. 0

The level of lactates and pyruvates in arterial blood of 35 patients with myocardial infarction without shock (17-without heart insufficiency and 18-with manifested but in various degrees) is higher as compared with the level of 18 healthy subject and the elevation is better manifested in the patients with cardiac insufficiency. The highest level of lactates and pyruvates is reached in the first 48 hours of the onset of the disease, after which they decrease progressively and in patients without cardiac insufficiency is normalized by the 5-6th day and in those with insufficiency-remains elevated. Slight to moderate correlation exists between the level of lactates and BE and PaCO2. Lacate and pyruvate level reoresents a more sensitive index for the existence of distrubances in the tissue metabolism as compared with the indices of alkaline-acid equilibtrium.
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PMID:[Metabolic disorders in the acute stage of cardiac infarction]. 0 32


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