title: Resetting of regional preload due to ventricular shape change alters diastolic and systolic performance.
abstract: The diastolic and systolic pressure of one ventricle is increased by an increase in volume and/or pressure of the opposite ventricle; however, a mechanism for the ventricular interaction remains unclear. We hypothesized that the shape change of one ventricle elicited by the opposite ventricle would lead to resetting of the regional length, which may explain the ventricular interaction. We used 15 cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were independently controlled. Diastolic regional segment area was calculated by multiplying circumferential and longitudinal lengths on right ventricular free wall (RVFW; n = 6), interventricular septum (IVS; n = 11), and left ventricular (LV) FW (n = 12). The regional area at relatively small volumes of both ventricles were expressed as 100%. With constant RV volume, increasing LV from 7 to 19 ml increased RV diastolic and systolic pressures by 2.7 and 5.5 mmHg, respectively. Conversely, increasing RV volume increased LV diastolic and systolic pressures by 2.3 and 7.5 mmHg, respectively. Increasing LV volume increased RVFW regional area from 121.0 to 124.6% (P < 0.01) and increased IVS regional area from 103.3 to 108.7% (P < 0.01), whereas the RV volume was held constant. Increasing RV volume also increased LVFW and IVS regional areas from 109.9 to 111.6% (P < 0.01) and from 106.8 to 108.9% (P < 0.05), respectively. Ventricular shape change elicited by ventricular interaction will increase the regional wall area, even though the volume of the chamber is unchanged. The increase in the regional area alters the position of the tissue on its resting and active length-tension relations and, thus, leads to enhancement of the chamber pressure.
authors.affiliation: First Department of Internal Medicine, Yamagata University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Yamaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Tamada
authors.forename: H
authors.initials: H
authors.lastname: Miyawaki
authors.forename: Y
authors.initials: Y
authors.lastname: Niida
authors.forename: A
authors.initials: A
authors.lastname: Fukui
authors.forename: M
authors.initials: M
authors.lastname: Shirakabe
authors.forename: I
authors.initials: I
authors.lastname: Ohta
authors.forename: K
authors.initials: K
authors.lastname: Tsuiki
authors.forename: H
authors.initials: H
authors.lastname: Tomoike
mesh_terms: D000818:Animals; D001021:Aortic Valve / Q000502:physiology; D003971:Diastole / Q000502:physiology*; D004285:Dogs; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles / Q000033:anatomy & histology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D013599:Systole / Q000502:physiology*; D016276:Ventricular Function