Active force during hypoxia of hypertrophied rabbit right ventricular trabeculae

Hypertrophy is often accompanied by increased myocardial oxygen demand, but any unique effects of hypoxia on contraction in hypertrophy are unknown. Trabeculae from normal [n = 9; 0.119 +/- 0.014 mm2 (means +/- SE) cross-sectional area] and hypertrophied (pulmonary artery constriction; n = 7; 0.108 +/- 0.028 mm2) rabbit right ventricles were subjected to graded hypoxia (Krebs-Ringer solution, 28 degrees C, 1 Hz stimulus frequency). During normoxia, peak active isometric (Pmax) and resting stress (Prest) at optimum length and peak rate of stress development (dP/dt) in hypertrophy were the same as normal and time to peak stress was longer than normal. Time to peak stress and dP/dt decreased with hypoxia, but time to peak stress remained longer than normal in hypertrophy; Prest was unchanged. The ratio of peak active stress (P) during hypoxia to Pmax decreased linearly with superfusate PO2, but the hypertrophy relationship (y = 4.00 X 10(-3) x + 0.084) is the same as normal (y = 3.70 X 10(-3) x + 0.154; p greater than 0.05). Therefore, a normal level of P was preserved in hypertrophied myocardium and prolonged time to peak stress might have been important for that preservation.