title: Effect of ventricular contraction, pressure, and wall stretch on vessels at different locations in the wall.
abstract: A cylindrical model of the heart was used to calculate the influence of ventricular filling and (isovolumic and isobaric) contraction on the cross-sectional area and resistance of a subendocardial and subepicardial maximally dilated arteriole and venule. Contraction is defined as the difference between static diastole and static systole. Furthermore, a small piece of rectangular myocardium containing the vessel was modeled to distinguish between the individual contributions of contractility (i.e., myocardial elastic properties), ventricular pressure, and local circumferential stretch to the changes in vascular area and resistance during contraction. Calculations were performed assuming the muscle fibers ran in either an apex-to-base or a circumferential direction. The results were similar for the two directions. Assuming constant, physiological arteriolar and venular pressures of 45 and 10 mmHg, respectively, coronary blood vessels were predicted not to collapse during ventricular contraction. Moreover, vascular area reduction was found to be larger for the arteriole (approximately 50%) than for the venule (approximately 30%) during both isovolumic and isobaric contractions. Consequently, arteriolar resistance was found to increase more than venular resistance (approximately 340 and 120%, respectively). Subendocardial area reductions were found to be somewhat smaller than subepicardial area reductions for the venule (by approximately 10%) but not for the arteriole. Contractility was found to be the main contributor to the changes in vascular area and resistance in the subepicardium but to contribute by < 50% to the changes in the subendocardium. Because pressure does, but stretch does not, contribute to the area change during isovolumic contraction and the reverse is true during isobaric contraction, it was concluded that although changes in vascular area and resistance may be similar for different contractions, the causes for these changes are very different.
authors.affiliation: Laboratory for Physiology, Vrije Universiteit, Amsterdam, The Netherlands.
authors.forename: M A
authors.initials: MA
authors.lastname: Vis
authors.forename: P H
authors.initials: PH
authors.lastname: Bovendeerd
authors.forename: P
authors.initials: P
authors.lastname: Sipkema
authors.forename: N
authors.initials: N
authors.lastname: Westerhof
mesh_terms: D001160:Arterioles / Q000502:physiology; D001810:Blood Volume; D003331:Coronary Vessels / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006801:Humans; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D010812:Physical Stimulation; D011312:Pressure; D016276:Ventricular Function; D014699:Venules / Q000502:physiology