Work and oxygen consumption of isolated right ventricular papillary muscle in experimental pulmonary hypertension

Right‐sided myocardial mechanical efficiency (work output/metabolic energy input) in pulmonary hypertension can be severely reduced. We determined the contribution of intrinsic myocardial determinants of efficiency using papillary muscle preparations from monocrotaline‐induced pulmonary hypertensive (MCT‐PH) rats. The hypothesis tested was that efficiency is reduced by mitochondrial dysfunction in addition to increased activation heat reported previously. Right ventricular muscle preparations were subjected to 5 Hz sinusoidal length changes at 37°C. Work and suprabasal oxygen consumption (V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$) were measured before and after cross‐bridge inhibition by blebbistatin. Cytosolic cytochrome c concentration, myocyte cross‐sectional area, proton permeability of the inner mitochondrial membrane and monoamine oxidase and glucose 6‐phosphate dehydrogenase activities and phosphatidylglycerol/cardiolipin contents were determined. Mechanical efficiency ranged from 23% to 11% in control (n = 6) and from 22% to 1% in MCT‐PH (n = 15) and correlated with work (r2 = 0.68, P