Use of M‐mode echocardiography in clinical pharmacology.

Gibson, D G

doi:10.1111/j.1365-2125.1979.tb00984.x

Cited by 10 publications

(3 citation statements)

References 38 publications

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“…The only echocardiographic evidence of such activity was a small increase in stroke volume. The intersubject variability in this value (Figure 2) was, however, quite marked and this probably reflects one of the cautionary notes made by Gibson (1979): the derivation of stroke volume from end-systolic and end-diastolic diameters involves the process of cubing and this may introduce considerable mathematical errors.…”

Section: Discussionmentioning

confidence: 92%

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Haemodynamic effects of BM 10.188, a new orally active inotropic agent, in healthy volunteers.

Whiting¹,

Kelman²,

Sumner³

et al. 1982

Brit J Clinical Pharma

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Section: Discussionmentioning

confidence: 92%

“…These noninvasive techniques-as they relate to drug studieshave been usefully reviewed by Gibson (1978Gibson ( , 1979.…”

Section: Discussionmentioning

confidence: 99%

Haemodynamic effects of BM 10.188, a new orally active inotropic agent, in healthy volunteers.

Whiting¹,

Kelman²,

Sumner³

et al. 1982

Brit J Clinical Pharma

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“…However, in the presence of changing cardiac dimensions the geometric assumptions underlying the derivation of some of these echo variables may change, and their validity has been rightly questioned (Gibson, 1979). Under these circumstances, in addition to cardiac dimension measurements, those measurements which avoid geometric assumptions (%Ad, VCf) are most likely to remain valid, and are most useful in estimating cardiac function (Fortuin & Pawsey, 1977).…”

Section: Discussionmentioning

confidence: 99%

Disopyramide and lignocaine. A comparison of cardiac effects using echocardiography.

Martin¹,

Bax²,

Tucker³

et al. 1980

Brit J Clinical Pharma

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1 The cardiac effects of disopyramide (D) and lignocaine (L) were measured and compared in normal volunteers (D n = 4; L n = 3) following the establishment of a series of three steady-state drug plasma concentrations spanning the therapeutic range (1.5-5 ig base ml-1). 2 During control and steady-state periods multiple measurements were made of heart rate, blood pressure, drug concentrations and echocardiographic measurement of cardiac dimensions and estimated left ventricular function. 3 No change in heart size or estimated function occurred with L except for a small increase in estimated cardiac output ( + 0.5 1 minm 1) secondary to a small rise in heart rate (maximum + 7 beats min-1). Blood pressure rose slightly (maximum + 11 mmHg).4 D caused an increase in heart size, marked at end systole (+ 0.63 cm), and a decrease in echo indices of ventricular function (25-33%). These changes were related to plasma drug concentration but were not reflected in cardiac output estimation since heart rate rose (+ 15 beats min 1) Blood pressure also rose ( +10 mmHg). 5 Significant differences were shown between D and L at similar plasma drug concentrations. The negative inotropic effect of D may be greater than previously suggested and clinically important.

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Pharmacodynamic Evaluation: Cardiovascular Methodologies

Mey

Hinder

2011

Drug Discovery and Evaluation: Methods in Clinical Pharmacology

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Use of M‐mode echocardiography in clinical pharmacology.

Cited by 10 publications

References 38 publications

Haemodynamic effects of BM 10.188, a new orally active inotropic agent, in healthy volunteers.

Haemodynamic effects of BM 10.188, a new orally active inotropic agent, in healthy volunteers.

Disopyramide and lignocaine. A comparison of cardiac effects using echocardiography.

Pharmacodynamic Evaluation: Cardiovascular Methodologies

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