Systolic coronary flow impediment in the dog: Role of ventricular pressureand contractility

Citation
P. Pagliaro et al., Systolic coronary flow impediment in the dog: Role of ventricular pressureand contractility, EXP PHYSIOL, 83(6), 1998, pp. 821-831
Citations number
23
Categorie Soggetti
Physiology
Journal title
EXPERIMENTAL PHYSIOLOGY
ISSN journal
09580670 → ACNP
Volume
83
Issue
6
Year of publication
1998
Pages
821 - 831
Database
ISI
SICI code
0958-0670(199811)83:6<821:SCFIIT>2.0.ZU;2-1
Abstract
The present study was planned to investigate the effect of left ventricular pressure and inotropic state on coronary arterial inflow in systole in the anaesthetized dog. A wide range of left ventricular systolic pressures, in cluding the physiological range, were studied. Experiments were done under conditions of maximal vasodilatation and low perfusion pressure in order to avoid vascular autoregulative interference and to keep the microvascular p ressure within the normal range. In five anaesthetized dogs, perfused with extracorporeal circulation system, ventricular volume was changed from 20 t o 50 mi in steps of 10 mi by filling an intraventricular latex balloon, and the related changes in left ventricular pressure and coronary flow were me asured. The volume was then extended to 70 mi to obtain an overstretch whic h induced a transient decrease in cardiac contractility. During the period of low cardiac contractility the volume was brought back to 20 mi in steps of 10 mi. Systolic ventricular pressure changed with volume but was lower d uring the period of low contractility. For systolic pressures below 100 mmH g there was no significant relationship between pressure and coronary systo lic flow, but the relationship shifted to higher flows during low contracti lity. For systolic pressures above 100 mmHg systolic coronary flow decrease d significantly when systolic pressure increased. In this case the slopes o f the relationships were not significantly different before and after the r eduction in contractility. These findings suggest that for systolic pressur es less than 100 mmHg (i.e. below the physiological range) the shielding ef fect of the contracting ventricle prevents the ventricular pressure from be ing transmitted in the myocardial wall. When systolic pressure exceeds 100 mmHg the shielding effect is overcome and the amplitude of the systolic flo w reduction varies with ventricular pressure.