INHIBITION OF THE CALCIUM PARADOX IN ISOLATED RAT HEARTS BY HIGH PERFUSATE SUCROSE CONCENTRATIONS

If a colloid osmotic (oncotic) pressure gradient develops across the m yocyte membrane during the calcium paradox, adding an oncotic agent to the perfusate should be inhibitory. After 10-min perfusion with Ca2+- free Krebs-Henseleit (KH) buffer under constant flow at 34 degrees C, myoglobin release was measured from Langendorff hearts reperfused with Ca2+-containing KH buffer. When the Ca2+-free medium contained 200 mM sucrose, myoglobin release was reduced to 5% of that observed in the absence of sucrose, a change that was not seen when 200 mosM NaCl, cho line chloride, LiCl, or glycerol was added. Replacement of 75 mM NaCl in the perfusate with 150 mM sucrose resulted in myoglobin release val ues that were 4% of the control. Plots of myoglobin release against su crose concentration under these hypertonic and isotonic conditions yie lded similar though separate curves. Sucrose also inhibited increases in wet weight-to-dry weight ratio and decreases in ATP and phosphocrea tine contents. These results support the hypothesis that an oncotic pr essure gradient arises during the calcium paradox at the moment of inc reased membrane permeability and plays a major role in its development .