title: Cardiac contraction affects deep myocardial vessels predominantly.
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.
authors.affiliation: Cardiovascular Research Institute, University of California, San Francisco 94143.
authors.forename: M
authors.initials: M
authors.lastname: Goto
authors.forename: A E
authors.initials: AE
authors.lastname: Flynn
authors.forename: J W
authors.initials: JW
authors.lastname: Doucette
authors.forename: C M
authors.initials: CM
authors.lastname: Jansen
authors.forename: M M
authors.initials: MM
authors.lastname: Stork
authors.forename: D L
authors.initials: DL
authors.lastname: Coggins
authors.forename: D D
authors.initials: DD
authors.lastname: Muehrcke
authors.forename: W K
authors.initials: WK
authors.lastname: Husseini
authors.forename: J I
authors.initials: JI
authors.lastname: Hoffman
mesh_terms: D000818:Animals; D001160:Arterioles / Q000502:physiology; D001464:Barium / Q000494:pharmacology; D001794:Blood Pressure; D002118:Calcium / Q000494:pharmacology; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology*; D004699:Endocardium / Q000166:cytology / Q000502:physiology; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000166:cytology; D011817:Rabbits; D013599:Systole
chemical_list: D001464:Barium; D002118:Calcium