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Figure 4 Butane-dione-monoxime (BDM) during demand ischemia. Ischemia (decreasing coronary perfusion pressure [CPP] to 20 mm Hg) reduced left ventricular systolic pressure (LVSP) to 62 mm Hg and left ventricular end-diastolic pressure (LVEDP) to 18 mm Hg. Tachycardia increased LVEDP to 28 mm Hg, indicating increased diastolic chamber stiffness. A 5 mmol/L BDM (5 mM) infusion imposed after tachycardia during sustained ischemic diastolic dysfunction progressively decreased LVSP from 62 to 43 mm Hg, indicating inhibition of calcium-activated myofilament cross-bridge cycling. However, elevated LVEDP was not simultaneously decreased, suggesting that it was not calcium-driven. Contractile function recovered after termination of infusion.