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Effect of propranolol on left ventricular function, segmental wall motion, and diastolic pressure-volume relation in man.

By J Coltart, E L Alderman, S C Robison and D C Harrison


Precise quantitation of the effects of the non-selective beta adrenergic blocking drug propranolol (3.15 mg/kg body weight) on left ventricular function, segmental wall motion, and diastolic pressure-volume relation in man has been performed. High fidelity left ventricular pressure measurements and simultaneous single-plane angiocardiograms were recorded on a video disc and volumes calculated by a light-pen computer system. Systolic segmental wall motion was computer analysed using the long axis-quadrasection method. Patients were transvenously atrially paced to maintain a constant heart rate. The haemodynamic effects of propranolol may vary depending upon the extent of pre-existing myocardial disease. In some patients ventricular function, as measured by ejection fraction, may be reduced. This reduction in ejection fraction appears to result from overall reduction in segmental wall motion, but also from accentuation of segmental wall abnormalities. These results are consistent with the thesis that beta adrenergic blocking drugs may inhibit compensatory sympathetic mechanisms. The diastolic effects of propranolol may include quite substantial increases in ventricular volumes in those patients with impaired cardiac function. With respect to the intact human ventricle, propranolol may increase diastolic volume for a given level of ventricular pressure. Thus, in a static sense, the ventricle in these patients could be viewed as being more compliant after propranolol administration. However, the fact that the length-tension relation, as measured by the slope of the logarithmic pressure versus volume plot is unaltered by propranolol, suggests that the muscle comprising the ventricle itself exhibits no alteration in its passive elastic properties

Topics: Research Article
Year: 1975
DOI identifier: 10.1136/hrt.37.4.357
OAI identifier:
Provided by: PubMed Central
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