Myocardial elasticity and left ventricular distensibility as related to oxygen deficiency and right ventricular filling. Analysis in a rat heart model.
Hypoxia-induced changes in diastolic left ventricular (LV) pressure volume (P-V) relationships and myocardial elasticity as well as the extent to which diastolic right ventricular (RV) interactions are involved under hypoxia were analysed in male open-chest Wistar rats under isovolumetric conditions. Wall stress sigma and differential elastic modulus E were calculated for the midwall region, assuming a spherical model. LV end-diastolic P-V relationship shifted significantly to the left only 2 min after the start of pure N2 ventilation. The slope of the E-sigma curve did not change, corresponding to the "contracture type" of decreased myocardial distensibility. Identical changes occurred when filling of the RV was increased under O2 ventilation. Hypoxia, under emptied RV, led within 8 min to substantially lower, non-significant steepening of the end-diastolic P-V relationships. There was a significant change in the diastolic P-V curve along with a parallel increase in stiffness constant b, 45 min after N2 ventilation and under emptied RV. However, as a result of failure of cardiac function, ischemia was by now prevailing. These findings led to the following conclusions: In the early phase of hypoxia, i.e. within the first 20 min (in the model used in the present study) no substantial rigor occurs but the increase of LV end-diastolic P-V values is essentially due to augmented RV filling, even under opened chest and removed pericardium. The geometrical influence of the RV mimics the "contracture type" of decreased myocardial distensibility and cannot be recognized on the basis of the E-sigma relationship. Without knowledge of RV pressure it is not feasible to distinguish early "contracture" or rigor from extraventricular influences, caused by changes in the filling of the neighbouring ventricle.
D000818:Animals; D001794:Blood Pressure; D003327:Coronary Disease / Q000503:physiopathology; D003971:Diastole; D004195:Disease Models, Animal; D004548:Elasticity; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors