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Diastolic ventricular interdependency in hypertrophied rat myocardium
Author(s) -
Lamberts Regis Raoul,
Stienen Ger M.J.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1199-a
Subject(s) - medicine , cardiology , diastole , muscle hypertrophy , volume overload , right ventricular hypertrophy , pressure overload , left ventricular hypertrophy , diastolic function , ventricular hypertrophy , ventricular pressure , blood pressure , cardiac hypertrophy , pulmonary hypertension , heart failure
Right ventricular (RV) hypertrophy is a consequence of RV pressure overload in pulmonary and congenital hearts diseases. Cardiac dysfunction under these circumstances has generally been attributed to a change in RV function. However, direct ventricular interdependency, due to the anatomical association, could be involved as well. Therefore, in control and monocrotaline (MCT)‐induced RV‐hypertrophied Langendorff rat hearts, we measured left ventricular (LV) and RV pressure‐volume relations simultaneously and determined ventricular interdependency. After 28 days, MCT (30 mg/kg) resulted in marked RV‐hypertrophy (RV weight: 220±15 to 437±34 mg in control and MCT, respectively, p<0.05) and in steeper diastolic and systolic RV pressure‐volume relations. An increase in LV volume increased RV diastolic pressure to a similar extent in the control and MCT group. Linear regression analysis of RV‐LV diastolic pressure relations yielded: slope 0.093±0.029 to 0.126±0.009, p>0.05 and intercept 2.68±0.14 to 4.19±0.08 mmHg, p<0.05, control and MCT, respectively. An increase in RV volume caused an increase in LV diastolic pressure in the MCT but not in the control group. Linear regression analysis of LV‐RV diastolic pressure relations yielded: slope 0.040±0.015 to 0.083±0.004, p<0.05, control and MCT, respectively. Peak RV and LV systolic pressure‐volume relations were not altered by changes in LV or RV volume, respectively. In conclusion, in hearts with MCT‐induced RV‐hypertrophy, ventricular interdependency caused LV diastolic dysfunction during compensated RV‐hypertrophy.