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PubMed1986

Beta adrenergic influence on oesophageal peristalsis in man.

The effects of the beta-1 adrenergic agonist prenalterol and the beta-2 adrenergic agonist terbutaline on oesophageal peristalsis were studied in nine healthy volunteers with pressures recorded in the proximal, middle, and distal oesophagus. Two doses of the agonists were given after pretreatment with placebo, propranolol, or metoprolol in a double blind randomised fashion. Terbutaline 0.25 +/- 0.25 mg iv decreased peristaltic pressure in middle oesophagus from 8.1 +/- 1.1 to 5.1 +/- 0.8 kPa (p less than 0.01) and in the distal oesophagus from 9.5 +/- 1.0 to 4.7 +/- 0.6 kPa (p less than 0.001). Peristaltic velocity was decreased in the distal oesophagus after terbutaline from 3.3 +/- 0.2 cm/sec to 2.9 +/- 0.2 cm/sec (p less than 0.05). Prenalterol 1 mg iv was followed by a decrease of peristaltic pressure in the middle oesophagus from 10.2 +/- 1.3 to 7.7 +/- 1.1 kPa (p less than 0.01) and a decrease of peristaltic velocity in upper oesophagus from 3.6 +/- 0.2 to 3.3 +/- 0.1 cm/sec (p less than 0.05) while no significant changes were seen in the distal oesophagus. Pretreatment with the beta-1 blocker metoprolol 15 mg iv blocked the effects of prenalterol 1 mg iv but not the effects of terbutaline. Propranolol 10 mg iv blocked the effects of terbutaline on peristaltic pressure. After metoprolol infusion mean distal peristaltic amplitude was 11.9 +/- 0.8 kPa compared with 8.5 +/- 1.2 kPa after placebo (p less than 0.01). It is concluded that both beta-1 and beta-2 adrenoceptor stimulation significantly decrease oesophageal peristaltic pressure in man. The body of the oesophagus seems to be under beta adrenergic inhibitory influence under physiological conditions.

Adrenergic beta-Agonists↗
PubMed1975

Measurement of stroke volume from pulmonary artery pressure record in man.

Stroke volume was determined from the pulmonary artery pressure record by application of the pulse contour method. Pulmonary artery pressure records were obtained in 17 patients using a high fidelity catheter-tip pressure transducer and simultaneous measurements of cardiac output were obtained from indicator dilution curves. The formula used was SV = KP sa (i plus T s/Td) where Psa is the planimetered area beneath the systolic portion of the pulmonary artery pressure curve. Ts and Td are the durations of systole and diastole, and K is a constant. Stroke volume was altered by isometric handgrip exercise and/or pharmacological agents in 15 patients. Serial measurementswere made in 2 patients in acute pulmonary oedema after myocardial infarction. Comparison of a wide range of values of stroke volume by the pulse contour method with those obtained from dye dilution curves showed a good correlation (r plus 0.97, P smaller than 0.001) regression line y = 1.01 times - 0.47. Measurement of stroke volume from the pulmonary artery pressure contour is a technique of potential value in serial haemodynamic monitoring.

Blood Pressure↗
PubMed1976

Failure of ST segment elevation to predict severity of acute myocardial infarction.

Praecordial ST segment elevation was measured at 35 electrode positions in each of 40 patients admitted to a coronary care unit after acute transmural anterior myocardial infarction. Serial praecordial electrocardiographic maps were recorded to determine (a) the time course as well as reproducibility of measurements of ST segment alterations, and (b) the degree of correlation between the magnitude of ST segment elevation and the severity of infarction, as assessed clinically or by sequential estimations of serum creatine kinase activity. Large variations in ST segment elevation were found in different patients with a comparable degree of myocardial damage, and at intervals of as little as four hours in the same patient. These variations were greater than could be explained by technical factors, and were not related to apparent changes in the patients' clinical status. The patterns of release of myocardial creatine kinase showed that the time course of ST segment elevation was longer than the period of myocardial necrosis. No correlation was found between the myocardial infarct size as determined by enzyme release and the highest levels of ST segment elevation recorded. The findings suggest that ST segment elevation as measured by praecordial electrocardiographic mapping does not constitute a reliable index of the size or severity of myocardial infarcts in man.

Adult↗
PubMed1980

Haemodynamic effects of prenalterol in patients with coronary heart disease.

The haemodynamic effects of prenalterol, a new selective beta-1 adrenoreceptor agonist, have been studied in patients with coronary heart disease. The drug was administered intravenously in a dosage of 0.5 to 2.5 micrograms/kg body weight to 20 patients undergoing coronary angiography and to 10 patients with a recent myocardial infarction, who had clinical evidence of left ventricular dysfunction. Left ventricular performance was enhanced in both groups of patients--left ventricular dP/dt (max) increased by 33 per cent and the systolic time intervals, pre-ejection period, and the ratio of pre-ejection period and left ventricular ejection shortened by 28 and 21 per cent, respectively. Cardiac output and stroke volume increased with no change in heart rate nor in left ventricular filling pressure. These results indicate that prenalterol enhances the contractile state of the myocardium without altering heart rate, and suggest that prenalterol could be of value in the management of patients with coronary heart disease, who have impaired left ventricular function.

Adrenergic beta-Agonists↗
PubMed1982

Cardiovascular effects of prenalterol on rest and exercise haemodynamics in patients with chronic congestive cardiac failure.

?The cardiovascular effects of the cardioselective beta, agonist prenalterol have been studied in nine patients with severe chronic congestive cardiac failure and in six patients with left ventricular dysfunction resulting from previous myocardial infarction. In the patients with cardiac failure intravenous prenalterol in a dosage of 1.5 microgram/kg bodyweight increased the cardiac index from 1.8 +/- 0.1 to 21.+/- 0.1 1/min per m2 and the left ventricular ejection fraction from 22 +/- 3 to 28 +/- 3%. There was a modest but significant increase in heart rate from 76 +/- 3 to 87 +/- 4 beats/min. Systemic vascular resistance fell from 2285 +/- 51 to 2041 +/- 534 dynes s-1 cm-5. On exercise, the left ventricular filling pressure fell from 33 +/- 6 to 26 +/- 3 and both cardiac index and stroke index increased by 13% and 16%, respectively. There was no significant change in heart rate or systemic blood pressure. In the patients with left ventricular dysfunction, coronary sinus blood flow increased from 107 +/- 11 to 133 +/- 12 ml/min but the increase in myocardial oxygen consumption was small and not significant (11.6 +/- 1.2 and 14.5 +/- 1.9 ml/min). In all patients there was no evidence that prenalterol was arrhythmogenic.

Adrenergic beta-Agonists↗
PubMed1984

Acute intravenous and sustained oral treatment with the beta1 agonist prenalterol in patients with chronic severe cardiac failure.

Prenalterol, a beta1 agonist, was given in a single blind acute intravenous study to seven patients with cardiac failure (New York Heart Association class II and III). It was then given in a double blind crossover study of sustained oral prenalterol to six of them. As a result of dose titration studies the oral dose of prenalterol given was 100 mg twice a day in all patients. Erect bicycle sprint tests were performed to exercise tolerance before and after treatment had been started. Cardiac function was assessed at rest and during graded supine bicycle exercise by determining haemodynamic indices using a Swan-Ganz catheter and radionuclide left ventricular ejection fractions. In the intravenous study cardiac function was assessed at rest and during exercise after a control infusion of dextrose and after an infusion of 5 mg prenalterol. In the oral crossover study a placebo or prenalterol were given for two periods of two weeks; at the end of each period exercise tolerance was measured and cardiac function assessed at rest and during exercise. Throughout the study period there was no change in symptoms, medication, or exercise tolerance. Intravenous prenalterol significantly improved cardiac function; left ventricular ejection fraction and cardiac index increased and left ventricular filling pressure fell both at rest and during exercise. Sustained oral treatment with prenalterol, however, did not improve resting left ventricular filling pressure or left ventricular ejection fraction at rest or during exercise but did increase heart rate at rest, and mean blood pressure and peripheral vascular resistance at rest and during exercise; in fact, during exercise left ventricular filling pressure was significantly increased while cardiac index and stroke volume index were decreased by prenalterol. Sustained oral treatment with prenalterol did not have the beneficial effects on cardiac function produced by intravenous treatment and in fact had deleterious effect on the measured indices of cardiac function during exercise.

Administration, Oral↗
PubMed1984

Acute haemodynamic effects of oral prenalterol in severe heart failure.

The acute haemodynamic effects of oral prenalterol were studied in 14 patients with severe heart failure (NYHA class III) due to ischaemic heart disease. All had received treatment with digoxin, diuretics, and in most cases vasodilators. Prenalterol was administered at two hourly intervals to give cumulative doses of 20, 50, and 100 mg and mean plasma concentrations of 53, 97, and 175 nmol/l. Haemodynamic measurements were made two hours after each dose with Swan-Ganz catheterisation; cardiac output was measured by thermodilution. There were no significant changes in heart rate, mean arterial pressure, or pulmonary artery diastolic pressure after the drug. Cardiac index rose significantly after 50 mg and 100 mg prenalterol. Oral prenalterol has a beneficial short term haemodynamic effect in patients with severe heart failure. If this effect is sustained prenalterol may be of value in the long term management of patients with this disabling condition.

Adrenergic beta-Agonists↗
PubMed1985

Are the clinical benefits of oral prenalterol in ischaemic heart failure due to beta blockade? A six month randomised double blind comparison with placebo.

The clinical effects of the oral beta 1 partial agonist, prenalterol, were investigated in 37 patients (29 male, eight female; mean age 57 years) with chronic ischaemic left ventricular failure using a placebo controlled randomised double blind protocol over six months. All patients were limited by dyspnoea (New York Heart Association class III) despite treatment with digoxin and diuretics. Twenty eight patients completed the protocol. Moderate clinical improvement was seen in the prenalterol group, whereas there was little change in the placebo group. Bicycle exercise capacity increased over six months in the prenalterol and placebo groups but only achieved statistical significance for prenalterol when compared with baseline values. Maximum exercise heart rate was significantly reduced in the prenalterol group compared with placebo. Radionuclide left ventricular ejection fraction at rest and during exercise and cardiothoracic ratio showed no significant improvement in either group over six months. Prenalterol was well tolerated and produced no increase in frequency of angina or ventricular arrhythmias. Prenalterol produced clinical benefits and improved exercise tolerance while reducing exercise heart rate. A moderate placebo response was noted. The apparent beta blocking effect of prenalterol may be as important as the beta 1 agonist effect in producing these benefits. Prenalterol has, however, been withdrawn because of side effects in animals.

Adrenergic beta-Agonists↗
PubMed1975

Orthostatic hypotension associated with paroxysmal ventricular tachycardia.

Two patients (aged 46 and 49 years) are presented who gave a history of several years' duration of unsteadiness, dizziness, and syncopal attacks on standing. Both had orthostatic hypotension which was associated with the development of a unifocal paroxysmal ventricular tachycardia. There was no evidence of organic heart disease. In one of the patients the symptoms usually developed when standing after working in a crouched position. He responded to treatment with beta-adrenergic blockade. The other patient developed her symptoms on standing, after exercise or other stress. The paroxysmal ventricular tachycardia, which occurred in the upright position only, was accompanied by a marked rise in plasma adrenaline. In this patient one contributory factor was a low blood volume and she responded to plasma volume expansion. We wish to draw attention to the common neurological symptoms with which paroxysmal ventricular tachycardia may present. We suggest that paroxysmal ventricular tachycardia may result from ventricular sensitivity to circulating adrenaline and not due to aberrant innervation of the heart as has been suggested previously.

Autonomic Nervous System↗
PubMed1976

An eighteen months' study of the clinical response to metoprolol, a selective beta1-receptor blocking agent, in patients with angina pectoris.

Following an initial dose response study, metoprolol, a selective beta1-receptor blocking agent, was compared with equipotent dosages of propanolol in a double blind cross-over study, including exercise tolerance tests, on fourteen patients with angina pectoris. Long term therapy with metoprolol then followed until the seventy-second week. Patients performed 8% more total work on metoprolol with 15% more work recorded up to the onset of S-T depression, in comparison with propranolol. In the long term, ther was no significant difference in work performed when the daily dosage of metoprolol was changed from a q.i.d. to a b.d. regime. Metoprolol was shown to be an effective anti-anginal compound with good tolerance and safety, with gradual improvement in underlying myocardial ischaemia during long term treatment.

Adrenergic beta-Antagonists↗
PubMed1976

The effect of beta-adrenoreceptive antagonists on the morbidity and mortality in cardiovascular disease.

The effect is critically reviewed of chronic administration of beta-adrenoreceptor antagonists on morbidity and mortality in angina pectoris and myocardial infarction. There is inconclusive evidence that the abrupt cessation of therapy with these agents may increase morbidity and mortality in angina pectoris. The type of anginal patient in which this may occur is not yet defined and neither is the mechanism. There is no evidence that beta-antagonists prolong the life of anginal patients. In the acute phase of experimental myocardial infarction, these drugs reduce mortality but do not do so in man. There is increasing evidence that they prolong life if administered to patients surviving the acute phase of myocardial infarction. The need for further studies is discussed.

Adrenergic beta-Antagonists↗
PubMed1975

Comparative effects of beta adrenergic blocking drugs.

Although many different beta blockers are now in clinical use, there is very little information concerning their relative efficacy, and it is still not clear what clinical importance should be attached to properties such as positive inotropic stimulation (intrinsic sympathomimetic activity or ISA) and membrane stabilizing action ("local anaesthetic effect" or "quinidine-like effect"). In this report we compare the ability of patients with angina to exercise on a bicycle ergometer while receiving a series of commonly used beta blockers, and attempt to determine the importance of ISA. The investigation is in four parts with the drugs given orally or intravenously: statistical analysis of the results was carried out using standard methods, both parametric and non-parametric (Friedmann analysis of variance, Wilcoxon matched pairs signed ranks test) by two independent statisticians. The relevant properties of drugs included in this paper are summarized in Table I. Laboratory reports using many different animal preparations may differ from this assessment under specific conditions, and the Table is intended only as a guide to the generally accepted properties of these drugs when used clinically. Results for sotalol are included for reference in the first part of this paper but the drug was withdrawn from clinical use and was not studied further.

Administration, Oral↗