Omachi A, Kleps R A, Henderson T O, Labotka R J
Department of Physiology and Biophysics, Graduate College, University of Illinois, Chicago 60680.
Am J Physiol. 1994 May;266(5 Pt 2):H1729-37. doi: 10.1152/ajpheart.1994.266.5.H1729.
If a colloid osmotic (oncotic) pressure gradient develops across the myocyte membrane during the calcium paradox, adding an oncotic agent to the perfusate should be inhibitory. After 10-min perfusion with Ca(2+)-free Krebs-Henseleit (KH) buffer under constant flow at 34 degrees C, myoglobin release was measured from Langendorff hearts reperfused with Ca(2+)-containing KH buffer. When the Ca(2+)-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, choline chloride, LiCl, or glycerol was added. Replacement of 75 mM NaCl in the perfusate with 150 mM sucrose resulted in myoglobin release values that were 4% of the control. Plots of myoglobin release against sucrose concentration under these hypertonic and isotonic conditions yielded similar though separate curves. Sucrose also inhibited increases in wet weight-to-dry weight ratio and decreases in ATP and phosphocreatine contents. These results support the hypothesis that an oncotic pressure gradient arises during the calcium paradox at the moment of increased membrane permeability and plays a major role in its development.
如果在钙反常过程中跨心肌细胞膜形成胶体渗透压（oncotic）梯度，那么向灌注液中添加一种胶体渗透压剂应该具有抑制作用。在34℃恒流条件下用无钙的克雷布斯 - 亨塞尔特（KH）缓冲液灌注10分钟后，测量用含Ca²⁺的KH缓冲液再灌注的Langendorff心脏中肌红蛋白的释放量。当无钙培养基含有200 mM蔗糖时，肌红蛋白释放量降至无蔗糖时观察值的5%，而添加200 mosM NaCl、氯化胆碱、LiCl或甘油时未出现这种变化。用150 mM蔗糖替代灌注液中的75 mM NaCl，导致肌红蛋白释放值为对照值的4%。在这些高渗和等渗条件下，肌红蛋白释放量与蔗糖浓度的关系图产生了相似但不同的曲线。蔗糖还抑制了湿重与干重比值的增加以及ATP和磷酸肌酸含量的降低。这些结果支持了这样的假设，即在钙反常过程中，在膜通透性增加的时刻会出现胶体渗透压梯度，并在其发展过程中起主要作用。
