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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In animals without myocardial infarction the new beta-sympathicolytic agent atenolol (4-[2'-hydroxy-3'-iso-propylaminopropoxy]-phenyl acetamide, ICI 66 082) dose-dependently decreased heart rate, systolic aortic pressure and cardiac output. Coronary mean flow, coronary resistance, stroke volume, left ventricular enddiastolic pressure and total peripheral vascular resistance did not change significantly. Atenolol significantly reduced myocardial contractility, expressed by (dp/dtmax), Vpm, t-(dp/dtmax) and pre-ejection period. Furthermore, the comparative studies in animals with myocardial infarction and concomitant reduced cardial efficiency revealed, that atenolol has neither a positive intrinsic activity as has practolol nor a negative intrinsic activity as has propranolol. The dose-contractility relation of atenolol resembles that of practolol: in low dosages a strong decrease is achieved, in higher dosages no further reduction of the contractility parameters is observed. Because of the strong negative inotropic and blood pressure lowering effect it is suggested to use atenolol only with great caution in patients with reduced cardiac efficiency.
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PMID:[The effect of atenolol on contractility and hemodynamics of the infarcted heart in comparison to propranolol and practolol (author's transl)]. 124 85

To find out what role, if any, beta 2-adrenoceptors play in cardiac contractility, the heart rate, stroke volume and cardiac output of twelve healthy male and female volunteers (aged 18-28 years) were studied at rest (standing) and during two stages of treadmill exercise, 2 h after ingestion of propranolol (100 mg) or atenolol (100 mg) or a placebo, on different occasions, in a double-blind crossover manner. Cardiac output was measured by a carbon dioxide-rebreathing method. Atenolol and propranolol caused equal reductions in heart rate at rest, and in heart rate and cardiac output during exercise (p less than 0.001, two-way analysis of variance). Neither atenolol nor propranolol had any significant effect on resting cardiac output, resting stroke volume or stroke volume during exercise. Since atenolol (100 mg) has been shown to be beta 1-adrenoceptor-selective, we conclude that cardiac inotropic function during exercise is largely beta 1-adrenoceptor-mediated with little or no beta 2-adrenoceptor involvement.
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PMID:Cardiac beta 2-adrenoceptors and the inotropic response to exercise in man. 168 99

1. We have utilised a new non-imaging echo-Doppler cardiac output device, using the principle of attenuated compensated volume flow (ACVF), to assess the cardiovascular effects of atenolol and buccal nitroglycerin (NTG) in a placebo-controlled study of 30 patients with coronary disease. 2. Atenolol (4 mg i.v.) reduced heart rate, cardiac output and time-averaged mean aortic velocity (P less than 0.01) and increased systemic vascular resistance (P less than 0.01). 3. Buccal NTG (5 mg) reduced systemic mean arterial pressure (P less than 0.01), cardiac stroke volume (P less than 0.05) and stroke length (P less than 0.01). 4. Thus although both drugs reduced time-averaged aortic velocity (an index of cardiac performance), the concomitant reduction in cardiac stroke length and tachycardia suggested sub-optimal cardiac filling for buccal NTG, whereas for atenolol (with the associated increased systemic vascular resistance but unchanged stroke length) attenuation of sympathetic stimulation at cardiac beta-adrenoceptors. 5. The ACVF method of cardiovascular monitoring should prove useful in human pharmacodynamic studies.
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PMID:Pharmacodynamic monitoring during acute intervention in ischaemic heart disease using a new echo-Doppler device. 211 60

Pharmacological and radio-ligand binding studies have recently indicated the existence of beta 2-adrenoceptors in the human heart. Their physiological role, however, remains to be elucidated. The present study investigated in 17 normal, young volunteers the effect on resting left ventricular (LV) function of two types of beta-blockers; a predominant beta 1-adrenoceptor antagonist (atenolol, 50 mg once daily) and ICI 118,551 (20 mg t.i.d.), a new, predominant beta 2-antagonist. LV function was assessed using M-mode echocardiograms and systolic time intervals. Atenolol, ICI 118,551, and placebo were given according to a randomized, double-blind, cross-over protocol. As compared with placebo, both drugs caused a decrease in resting heart rate, but the reduction by ICI 118,551 was less pronounced. Systolic blood pressure was only reduced by atenolol 8 mm Hg on average. Cardiac output was decreased to the same extent following treatment with atenolol (-20%) as after ICI 118,551 (-17%). These decreases in cardiac output were related to the beta-blocker-induced bradycardia, since stroke volumes were not affected during either selective beta 1- or beta 2-blockade. In addition, all other echocardiographic variables reflecting LV pump function, such as fractional shortening, velocity of diameter change and of displacements, pre-ejection period, and the ratio of PEP/LVET, were not different from placebo. We conclude that in normal young subjects, global LV pump function is not affected by beta 1- or by beta 2-blockade, despite the negative chronotropic effect of both drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of beta 1- versus beta 2-adrenoceptor blockade on left ventricular function in humans. 242 84

The cardiovascular effects of single oral doses of nifedipine (20 mg), atenolol (50 mg), or of their combination were compared with placebo in a double-blind randomized cross-over study in 10 normotensive volunteers. After subjects rested for 2 h, before drug administration, heart rate, blood pressure, stroke volume index, and cardiac index were measured noninvasively. These cardiovascular parameters were then determined prior to and after exercise periods (160 W, 10 min, bicycle ergometry) which were performed 40, 70, 130, 190, 310 min, and 22 h after drug intake. Nifedipine decreased resting diastolic blood pressure (p less than or equal to 0.05) after 2 h, whereas systolic blood pressure remained unchanged and heart rate significantly increased at rest and after exercise. Stroke volume index and cardiac index were unaffected. Atenolol significantly decreased systolic and diastolic blood pressure as well as heart rate; stroke volume index following exercise increased significantly, and cardiac index was unchanged. Administration of the combination caused a significantly more pronounced fall of systolic and diastolic blood pressure as compared with either drug alone, whereas the negative chronotropic effect was not different from that of atenolol. As did atenolol, the combination increased stroke volume index after exercise with no change in cardiac index. Maximum plasma concentrations of nifedipine (37.1 +/- 16.7 ng/ml) and atenolol (276.3 +/- 107.2 ng/ml) and terminal half-life of atenolol (9.9 +/- 2.6 h) were not altered by combined administration of the drugs.
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PMID:Interaction between nifedipine and atenolol: pharmacokinetics and pharmacodynamics in normotensive volunteers. 242 95

We compared exercise responses in two groups of hypertensive patients treated with an angiotensin converting enzyme (ACE) inhibitor (lisinopril, 20-80 mg/day, n = 17) or a cardioselective beta-blocker (atenolol, 50-200 mg/day, n = 9). Measurements were made at rest and during exercise at 25 W (2.7 mets) and at 50 W (3.8 mets) on a bicycle ergometer (where mets is exercising oxygen consumption/resting oxygen consumption) after 4 weeks of placebo, and again after 12 weeks of drug administration. Both drugs reduced (P less than 0.05) mean arterial pressure. Atenolol caused significant decreases in the heart rate (approximately 25%) and cardiac output (approximately 26%; Defares CO2 rebreathing), and significant increases in total peripheral resistance (approximately 30%) and arteriovenous O2 content (approximately 20%). Lisinopril decreased (P less than 0.05) stroke volume. At the same exercise intensity systolic blood pressure, arteriovenous O2 and total peripheral resistance were lower (P less than 0.05) and the heart rate was higher (P less than 0.05) after lisinopril than after atenolol. After the treatment of hypertension with the ACE inhibitor the responses to exercise were less restrictive than those after treatment with the cardioselective beta-blocker.
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PMID:Effects of angiotensin converting enzyme inhibition and beta-blockade on exercise responses in hypertensive patients. 285 65

The influence of chronic beta 1-adrenoceptor blockade on haemodynamic and metabolic responses was examined in eight young hypertensive subjects during a 40 min submaximal bicycle test at 50% of maximal capacity. The patients were randomly allocated to one placebo and one treatment period of 6 weeks. During treatment atenolol (Tenormin, 100 mg) was given twice daily. Arterial pressure, cardiac output, leg blood flow, oxygen uptake and different metabolites in the blood were determined. The heart rate was reduced by beta 1-adrenoceptor blockade by 30% during exercise, and the decrease was related to plasma concentration of the drug. Cardiac output was decreased by approximately 10%, but the negative chronotropic effect was partly compensated for by a higher stroke volume. Blockade leg blood flow was reduced by 10%, but more oxygen was extracted, giving an unchanged oxygen uptake. Blood concentration and leg uptake of glucose were not influenced by the treatment, but plasma free fatty acids were reduced by 30-40%. Leg lactate release was decreased to half the value in the unblocked situation. Plasma renin activity did not increase at the beginning of exercise, but after 40 min an increase was seen, though only to half of the pretreatment value. It is concluded that beta 1-adrenoceptor blockade during submaximal exercise reduces blood flow to the working muscles and that this reduction is the result of a lower cardiac output. Aerobic metabolism is unchanged as a result of increased oxygen extraction, but less fat is used as lipolysis is inhibited. Glucose uptake by the working muscles is unchanged by beta 1-blockade, but there is evidence for an increased carbohydrate metabolism. As for non-selective blockade, atenolol decreases lactate release but this could be the result of non-specific action on the beta 1-receptor and/or increased carbohydrate oxidation. Furthermore, the beta 1-adrenoceptors seem to have a major influence on the renin release during exercise.
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PMID:Haemodynamic and metabolic responses to prolonged exercise after chronic beta 1-adrenoceptor blockade in hypertensive man. 286 Sep 92

We evaluated maximal performance during cycle ergometry and treadmill exercise in 14 hypertensive male joggers treated with prazosin or atenolol in an unblinded, placebo-controlled, crossover design. Maximal oxygen uptake was measured during both exercise modalities; cardiac output was measured only during cycle ergometry using the acetylene rebreathing technique. Both drugs reduced resting systolic and diastolic blood pressures. Prazosin reduced total peripheral resistance during submaximal exercise but had little effect on maximal cycle and treadmill performance. Atenolol, in contrast, reduced treadmill duration, maximal oxygen uptake, and heart rate compared with placebo. Atenolol also increased stroke volume and the arterial venous oxygen difference and reduced cardiac output during cycle exercise. Both drugs produced similar reductions in exercise diastolic pressure, but exercise systolic pressure was lower only during atenolol treatment. Prazosin was better tolerated by the subjects and was preferred by 10 of the men. We conclude that both drugs effectively reduced resting blood pressure, but that atenolol decreased exercise cardiac output and may impede exercise performance in physically active hypertensive subjects.
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PMID:Effect of atenolol or prazosin on maximal exercise performance in hypertensive joggers. 291 65

Working capacity, left ventricular ejection fraction (EF), stroke volume and the phase of the left ventricular contraction were tested before and after 3 weeks of atenolol treatment in 14 patients with angina pectoris and coronary insufficiency diagnosed by thallium tomography. Eight patients (group A) increased their EF during exercise and six patients (group B) showed a decrease in EF when tested with placebo. When treated with atenolol the changes in EF during exercise were reversed in the two groups. Group B increased and group A decreased their EF. Atenolol caused an increase in working capacity in group B, but not in group A. In both groups atenolol caused an increased stroke volume and a decreased phase deviation at rest, while no significant volume changes or phase changes occurred during exercise. These results indicate that atenolol treatment had the most marked effect in patients with the most pronounced disease.
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PMID:The effect of atenolol on the left ventricular performance in patients with angina pectoris measured with isotope technique. 335 50

The haemodynamic effects of concomitant intravenous administration of disopyramide (Norpace) and atenolol (Tenormin) were studied in a cross-over trial in 7 patients with ischaemic heart disease. Following 150 mg disopyramide i.v. the cardiac index (CI) and stroke volume index (SVI) decreased by 14% and 26%, respectively and the heart rate (HR) and preejection period index (PEPI) increased by 13% and 19%, respectively. A decrease in CI of 14% and HR of 21%, respectively were noted after intravenous administration of 7.5 mg atenolol; PEPI increased by 10% whereas SVI remained unchanged. The cardiac Index (CI) fell by 33% following the administration of both drugs. The effect on CI of the two drugs was additive. The effect of disopyramide and atenolol on HR, SVI and PEPI was not significantly modified by coadministration of the other drug. No change in blood pressure was observed after disopyramide or atenolol. A correlation (rho) of 0.540 and 0.387 was observed between the change in PEPI and the log free and total serum concentrations of disopyramide, respectively. Combined intravenous use of the two drugs in patients with incipient or overt heart failure is not recommended, unless it is due to the arrhythmia to be treated.
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PMID:Haemodynamic effects and kinetics of concomitant intravenous disopyramide and atenolol in patients with ischaemic heart disease. 370 40


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