Related Experiment Videos
Cardiac contraction affects deep myocardial vessels predominantly
M Goto1, A E Flynn, J W Doucette
1Cardiovascular Research Institute, University of California, San Francisco 94143.
Insights
Cardiac contraction significantly impedes subendocardial blood flow more than subepicardial flow. This effect on myocardial flow is primarily due to intramyocardial forces, not left ventricular pressure.
Area of Science:
- Cardiovascular Physiology
- Myocardial Perfusion Dynamics
- Vascular Biology
Background:
- Myocardial blood flow is crucial for cardiac function.
- Understanding regional differences in flow is vital for diagnosing and treating heart conditions.
- Intramyocardial forces and ventricular pressure are potential regulators of coronary blood flow.
Purpose of the Study:
- To investigate the distinct roles of intramyocardial forces and systolic ventricular pressure on myocardial blood flow in different cardiac layers.
- To analyze the impact of systolic arrest versus diastolic arrest on subendocardial and subepicardial flow.
- To examine the structural characteristics of intramyocardial vessels in relation to myocardial layers and cardiac states.
Main Methods:
- Rabbit hearts were excised and perfused.
- Myocardial flow was measured during induced systolic arrest (low Ca2+, Ba2+ perfusion) and diastolic arrest (pentobarbital, cardioplegia).
- Left ventricular pressures of 60 and 0 mmHg were maintained during systolic arrest.
- Intramyocardial vessel number and size were assessed post-perfusion fixation.
Main Results:
- Subendocardial flow was lower than subepicardial flow during systolic arrest, irrespective of left ventricular pressure.
- During diastolic arrest, subendocardial flow exceeded subepicardial flow.
- Terminal arteriole and capillary diameters were significantly smaller in the subendocardium compared to the subepicardium during systolic arrest.
- Vessel densities did not differ between layers, but diameters were altered by cardiac state.
Conclusions:
- Cardiac contraction, driven by intramyocardial forces, predominantly constricts subendocardial vessels.
- This constriction leads to reduced subendocardial blood flow relative to subepicardial flow during systole.
- Left ventricular pressure has a lesser impact on this flow disparity compared to the mechanical effects of contraction.
Abstract:
To evaluate the roles of intramyocardial forces and systolic ventricular pressure in myocardial flow in the different layers separately, we measured myocardial flow in rabbit hearts during stable systolic contracture with left ventricular pressures of 60 (n = 5) and 0 mmHg (n = 5) and during stable diastolic arrest (n = 5). We also measured the number and size of the intramyocardial vessels after perfusion fixation (systolic arrest, n = 5; diastolic arrest, n = 5). In 25 rabbits, hearts were excised and perfused from the aortic root. Systolic arrest was achieved by perfusion of a low-Ca2+ Tyrode solution containing 2.0 mM Ba2+. Diastolic arrest was achieved by intraventricular injection of 700-1,000 mg pentobarbital sodium and was maintained by perfusion with St. Thomas cardioplegic solution. At perfusion pressure of 100 mmHg, subendocardial flow was lower than subepicardial flow during systolic arrest regardless of left ventricular pressure, whereas during diastolic arrest, subendocardial flow was higher than subepicardial flow. Subendocardial-to-subepicardial flow ratios for a physiological range of perfusion pressures were lower during systolic arrest with low rather than with high left ventricular pressure. Small arteriolar and capillary densities showed no difference between subendocardium and subepicardium. During systolic arrest, diameters of subendocardial terminal arterioles (4.6 +/- 1.3 microns) and capillaries (4.0 +/- 1.3 microns) were smaller than those in the subepicardium (8.8 +/- 1.7 and 7.1 +/- 1.6 microns, respectively; P less than 0.0001), whereas during diastolic arrest, diameters of subendocardial terminal arterioles (10.1 +/- 2.0 microns) and capillaries (7.6 +/- 1.8 microns) were slightly larger than those in the subepicardium (9.5 +/- 1.5 and 6.7 +/- 1.0 microns, respectively; P less than 0.01). We conclude that cardiac contraction predominantly affects subendocardial vessels and impedes subendocardial flow more than subepicardial flow regardless of left ventricular pressure.