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Contribution of extravascular compression to reduction of maximal coronary blood flow
1Department of Physiology, School of Medicine, University of South Carolina, Columbia 29208.
Insights
Ventricular compression significantly reduces coronary blood flow in maximally dilated arteries. Even at high pressures, the coronary system may store systolic arterial flow.
Area of Science:
- Cardiovascular Physiology
- Coronary Circulation
- Hemodynamics
Background:
- Ventricular compression's impact on coronary blood flow is crucial for understanding myocardial perfusion.
- Maximal vasodilation is a key state for assessing coronary flow dynamics under external pressure.
Purpose of the Study:
- To investigate the effects of left ventricular compression on left circumflex coronary artery blood flow.
- To quantify the relationship between ventricular pressure and coronary blood flow during maximal vasodilation.
Main Methods:
- Mongrel dogs under anesthesia were used, with the left circumflex artery perfused at constant pressure.
- Left ventricular pressure was experimentally altered, and adenosine was infused to achieve maximal vasodilation.
- Coronary flow was measured across a range of ventricular pressures and perfusion pressures.
Main Results:
- A linear decrease in coronary blood flow was observed with increasing peak ventricular pressure.
- Compressive forces were similar during systole and diastole, with left ventricular end-diastolic pressure contributing significantly to flow changes.
- Higher perfusion pressures reduced the impact of ventricular pressure on coronary flow and conductance.
Conclusions:
- Ventricular compression significantly impedes coronary blood flow, particularly at higher ventricular pressures.
- The data suggest an active storage mechanism within the dilated coronary system during systole.
- Coronary conductance is less affected by ventricular pressure at higher perfusion pressures.
Abstract:
Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.