Wisenbaugh T, O'Connor W N
Department of Medicine (Cardiology), Veterans Administration Medical Center, Lexington, Kentucky.
Am J Physiol. 1988 Jun;254(6 Pt 2):H1099-104. doi: 10.1152/ajpheart.1988.254.6.H1099.
To test the hypothesis that alterations in ventricular size and function may persist long after reversal of a severe pressure overload, right ventricular (RV) hypertrophy was produced in cats by abrupt, severe constriction of the pulmonary artery (PA) for 8 wk, after which pressure overload was completely reversed by surgical removal of the PA band (group III). Despite debanding and recovery from pressure overload (RV peak systolic pressure = 22 +/- 4 vs. 66 +/- 20 mmHg before debanding and 25 +/- 4 mmHg in controls), parameters of hypertrophy 8-10 mo later remained substantially increased: e.g., RV/LV (left ventricular) mass ratio was 0.36 +/- 0.06 in group III vs. 0.24 +/- 0.03 in controls (group I) and 0.43 +/- 0.07 in a separate cohort (group II) studied after 8 wk of banding. Maximum RV stroke work during volume loading was computed from RV micromanometry and PA electromagnetic flow: 20 +/- 8 g-cm/g for group III vs. 51 +/- 14 for group I, P less than 0.05, and 21 +/- 7 for group II. Thus severe pressure overload of the RV may produce changes in size and function that are not fully reversed by complete removal of the overload.