Steigen T K, Larsen T S
Department of Physiology, University of Tromsø, Norway.
Arctic Med Res. 1991;50 Suppl 6:53-7.
The phospholipid bilayer of the plasma membrane plays an important role in forming a functional barrier against leakage of ions and other cell constituents. We have examined the effect of an exogenously added phospholipase C (PLC) on phospholipid degradation in isolated rat myocardial cells subjected to hypothermia (5 degrees C) and hypothermia followed by rewarming to 37 degrees C. The activity of PLC was measured as glycerol output to the incubation medium since the combined action of PLC and endogenous lipases will result in glycerol production. Addition of PLC resulted in a significantly higher output of glycerol in rewarmed myocytes than in myocytes kept constantly at 5 degrees C and 37 degrees C. Rewarmed cells also showed the highest leakage of lactate dehydrogenase (LDH), but there was no additional effect of PLC on LDH leakage. Normal levels of cellular ATP were maintained in all myocyte groups. These results show that rewarming from hypothermia may cause structural derangements in the phospholipid bilayer of the sarcolemma which in turn could favor attack by endogenous phospholipases.
质膜的磷脂双分子层在形成防止离子和其他细胞成分泄漏的功能性屏障方面发挥着重要作用。我们研究了外源性添加的磷脂酶C（PLC）对处于低温（5℃）以及低温后复温至37℃的离体大鼠心肌细胞中磷脂降解的影响。由于PLC和内源性脂肪酶的联合作用会产生甘油，因此将PLC的活性测定为向孵育培养基中输出的甘油量。添加PLC后，复温后的心肌细胞中甘油的输出量显著高于一直保持在5℃和37℃的心肌细胞。复温后的细胞还表现出最高的乳酸脱氢酶（LDH）泄漏，但PLC对LDH泄漏没有额外影响。所有心肌细胞组的细胞ATP水平均维持正常。这些结果表明，低温复温可能会导致肌膜磷脂双分子层的结构紊乱，进而有利于内源性磷脂酶的攻击。
