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Biomedical subjects

B Silke

Publications and source records attributed to B Silke.

At least 163 records · Page 9Linked to original sources
PubMed1982

Intravenous beta-blockade in coronary heart disease: is cardioselectivity or intrinsic sympathomimetic activity hemodynamically useful?

Beta-blocking drugs are increasingly prescribed in coronary heart disease, but controversy surrounds the hemodynamic relevance of their ancillary pharmacologic properties--cardioselectivity and intrinsic sympathomimetic activity. We therefore compared the effects of four intravenous beta-adrenoreceptor antagonists with different ancillary properties on left ventricular function in 24 patients with coronary heart disease. All four drugs depressed the relation between left ventricular filling pressure and cardiac output at rest and during exercise. However, practolol and oxprenolol, which have intrinsic sympathomimetic activity, induced significantly less depression of left ventricular function than either propranolol or metoprolol, which do not have this activity. Cardioselectivity, a property of both practolol and metoprolol, had no discernible hemodynamic advantage. Beta-blocking drugs that have intrinsic sympathomimetic activity appear to be more effective in maintaining cardiac function than drugs without this property, when given intravenously to patients with coronary heart disease.

Adrenergic beta-Antagonists↗
PubMed1982

Comparative haemodynamic dose response effects of propranolol and labetalol in coronary heart disease.

The immediate haemodynamic dose response effects of beta blockade (propranolol: 2 to 16 mg) were compared with those of combined alpha beta blockade (labetalol: 10 to 80 mg) in a randomised study of 20 patients with stable angina pectoris. After control measurements, the circulatory changes induced by four logarithmically cumulative intravenous boluses of each drug in equivalent beta blocking doses were evaluated at rest, after which comparison of the effects of the maximum cumulative dose of each was undertaken during a four minute period of supine bicycle exercise. Propranolol, at rest, induced significant dose related reductions in heart rate and cardiac output, with reciprocal increases in the systemic vascular resistance and pulmonary artery occluded pressure; systemic arterial pressure was unchanged. Labetalol was followed by significant dose related decreases in systemic blood pressure and vascular resistance associated with a significant increase in cardiac output; heart rate and pulmonary artery occluded pressure were unchanged. The slope of the left ventricular pumping function curve relating output to filling pressure from rest to exercise was significantly depressed by propranolol but unchanged after labetalol. The less deleterious effects on left ventricular haemodynamic performance after alpha beta blockade in contrast to beta blockade alone in ischaemic heart disease may be attributable to the concomitant reduction in left ventricular afterload associated with the alpha blocking activity of labetalol.

Adult↗
PubMed1982

Circulatory dose-response effects of hydrochlorothiazide at rest and during dynamic exercise in essential hypertension.

The immediate and sustained circulatory effects of hydrochlorothiazide were evaluated at rest and during dynamic exercise in 24 patients with essential hypertension. Twenty-four hours after the first dose (50mg) there was a reduction in the resting systolic blood pressure, with attenuation of exercise tachycardia. During sustained therapy at two dose levels (50mg and 100mg), each of one month's duration, the systolic and diastolic blood pressure were reduced, both at rest and during dynamic exercise, without substantial difference between the two doses. Exercise tachycardia was attenuated during longterm treatment, without alteration of the pressor responses to exercise. The reduction in exercise tachycardia at the same workload in this study suggests that thiazides, in addition to their diuretic action, have a vascular component that augments the fall in systemic vascular resistance during dynamic exercise.

Adult↗
PubMed1981

Haemodynamic dose-response effects of i.v. metoprolol in coronary heart disease.

The haemodynamic effects of intravenous metoprolol, over the dose-range 2.5--20 mg, were studied in 12 patients with coronary heart disease. The pharmacodynamic activity of the drug was confirmed by the suppression of exercise systolic pressure and tachycardia. There were statistically significant dose-response reductions in systolic and diastolic pressures, heart rate and cardiac output together with a dose-related increase in pulmonary wedge pressure. In patients with coronary heart disease intravenous metoprolol should probably not exceed the doses used in this study and should be administered with caution in patients with impairment of pumping function.

Adult↗
PubMed1981

Speed of onset of pharmacodynamic activity of propranolol, practolol, oxprenolol and metoprolol after intravenous infection in man.

1 The speed of onset of the pharmacodynamic activity of intravenous propranolol, practolol, oxprenolol and metoprolol was determined, using attenuation of isoprenaline-induced tachycardia as the end-point, in 16 patients with clinically coronary heart disease. 2 Antagonism was evident within 15 s of injection into the central circulation of all four drugs. The time to maximum attenuation of isoprenaline tachycardia was significantly more rapid with propranolol and oxprenolol than with practolol and metoprolol.

Adrenergic beta-Antagonists↗
PubMed1981

Immediate and sustained haemodynamic effects of prazosin during upright exercise in man.

To ascertain the immediate pharmacodynamic and long-term haemodynamic effects of prazosin in chronic ambulant heart failure, measurements were made during sitting, standing, and walking in 12 patients with severe ischaemic left ventricular failure before and after their first dose of prazosin (2 mg) and in six of these patients after a further 12 weeks of sustained treatment (2 mg tds). When first added to treatment with digoxin and frusemide, prazosin was followed within an hour by substantial reductions in systemic arterial, pulmonary arterial, and pulmonary venous pressures in both postures at rest and also during walking. These changes were significantly attenuated after continued treatment. Cardiac output while sitting and standing at rest was reduced in both instances but the response to exercise was unchanged. The pharmacodynamic effects of prazosin in heart failure are explicable in terms of blockade of alpha1 adrenoceptors in arterial resistance and venous capacitance vessels augmented perhaps by lessening of reflex vasoconstriction secondary to the reduction in pulmonary venous pressure. The cause of the attenuation of the acute haemodynamic effects of the drug during sustained treatment is unknown.

Coronary Disease↗
PubMed1981

The pharmacokinetic, pharmacodynamic and haemodynamic effects of acute and chronic alpha-adrenoceptor blockade in chronic heart failure.

Pharmacokinetic and haemodynamic studies with the alpha-1 adrenoceptor antagonist prazosin were made in 20 patients disabled by chronic ischaemic heart failure. In eight patients given doubling doses of oral prazosin in successive days, the peak plasma concentration and area under the concentration-time curve were linearly reated to the oral dose. The pharmacodynamic response was a dose-related fall in the systemic arterial pressure, both supine and standing; dose-response effects were most evident in the upright posture. Severe hypotension occurred unpredictably, and was unrelated to co-existing clinical or radiographic features. There was a reciprocal relationship between the reduction in systemic blood pressure and the increase in heart rate. The immediate and long-term haemodynamic effects were determined during sitting, standing and walking in 12 patients before and after their first dose of prazosin (2 mg) and in 6 of these patients after a further 12 weeks of sustained treatment (2 mg t.d.s.). When first added to treatment with digoxin and frusemide, prazosin was followed by substantial reductions in systemic arterial, pulmonary arterial and pulmonary venous pressures in both postures at rest and also during walking. These changes were significantly attenuated after continued treatment. Cardiac output sitting and standing at rest was reduced in both instances but the response to exercise was unchanged. The pharmacodynamic effects of prazosin in heart failure are explicable in terms of blockade of alpha-1 adrenoceptors in arterial resistance and venous capacitance vessels; the cause of the attenuation of the acute haemodynamic effects of the drug during sustained treatment is less clearly defined.

Adrenergic alpha-Antagonists↗