title: The effects of asymmetric ventricular filling on left-right ventricular interaction in the normal rat heart.
abstract: Heart failure is characterised by ventricular dysfunction and with the potential for changes to ventricular volumes constraining the mechanical performance of the heart. The contribution of this interaction from geometric changes rather than fibrosis or metabolic changes is unclear. Using the constant pressure Langendorff-perfused rat heart, the volume interaction between left ventricle (LV) and right ventricle (RV) was investigated. RV diastolic stiffness (P < 0.001) and developed pressure (P < 0.001) were significantly lower than LV. When the RV was fixed at the end-diastolic volume (EDV) or EDV + 50 %, both LV systolic and diastolic performance were unaffected with increasing LV balloon volume. However, at fixed LV volume, RV systolic performance was significantly decreased when LV volume increased to EDV + 50 % when RV volume was increased incrementally between 50 and 300 μl (P < 0.001). Systolic interaction in RV was noted as declining RV peak systolic load with increasing LV systolic pressure (P < 0.05) and diastolic interaction was noted for RV when LV volume was increased from EDV to EDV + 50 % (P < 0.05). RV diastolic wall stress was increased with increasing LV balloon volume (P < 0.05), but LV wall stress was unaltered at fixed RV balloon volume. Taken together, increasing LV volume above EDV decreased systolic performance and triggered ventricular constraint in the RV but the RV itself had no effect on the performance of the LV. These results are consistent with overload of the LV impairing pulmonary perfusion by direct ventricular interaction with potential alteration to ventilation-perfusion characteristics within the lung.
authors.affiliation: School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.
authors.forename: Kimberley
authors.initials: K
authors.lastname: Pett
authors.forename: David
authors.initials: D
authors.lastname: Hauton
mesh_terms: D000818:Animals; D003971:Diastole; D006352:Heart Ventricles / Q000033:anatomy & histology*; D066298:In Vitro Techniques; D008297:Male; D015425:Myocardial Reperfusion; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume; D013599:Systole; D016276:Ventricular Function / Q000502:physiology*