Beckman J K, Owens K, Knauer T E, Weglicki W B
Am J Physiol. 1982 Apr;242(4):H652-6. doi: 10.1152/ajpheart.1982.242.4.H652.
The susceptibility of the lipids of canine cardiac sarcolemma to attack by soluble lysosomal lipases was studied to simulate in vitro the lipolytic injury that occurs during ischemia. The sarcolemmal fraction was incubated at 37 degrees C with the soluble portion of rat hepatic lysosomes (the lysosol) under conditions (pH 5.0, 5 mM ethylenediaminetetraacetic acid) appropriate for the activity of the major lysosomal lipases. Incubation of sarcolemma with lysosol resulted in a 78% lipolysis of sarcolemmal triacylglycerols, a lesser degradation of glycerophospholipids, and a parallel production of free fatty acids and lysophospholipids. The hydrolysis of sphingomyelin was negligible but was greatly stimulated (75%) by the addition of Triton X-100 (1 mg). Endogenous lipolytic activities of the sarcolemma did not contribute significantly to the observed lipid hydrolysis either in the presence or absence of detergent. The lipolysis of sarcolemmal triacylglycerols, glycerophospholipids, and sphingomyelin (Triton X-100 stimulated) were inhibited by varying concentrations of chlorpromazine. Thus cardiac sarcolemma is susceptible to hydrolysis of lysosomal lipases, and chlorpromazine inhibits this potentially injurious process.
为了在体外模拟缺血期间发生的脂解损伤，研究了犬心肌肌膜脂质对可溶性溶酶体脂肪酶攻击的敏感性。在适合主要溶酶体脂肪酶活性的条件（pH 5.0，5 mM乙二胺四乙酸）下，将肌膜部分与大鼠肝脏溶酶体的可溶性部分（溶胞液）在37℃孵育。肌膜与溶胞液孵育导致肌膜三酰甘油发生78%的脂解，甘油磷脂降解较少，同时游离脂肪酸和溶血磷脂平行产生。鞘磷脂的水解可忽略不计，但加入Triton X-100（1 mg）后受到极大刺激（75%）。无论有无去污剂，肌膜的内源性脂解活性对观察到的脂质水解均无显著贡献。不同浓度的氯丙嗪抑制了肌膜三酰甘油、甘油磷脂和鞘磷脂（Triton X-100刺激）的脂解。因此，心肌肌膜易受溶酶体脂肪酶水解的影响，氯丙嗪可抑制这一潜在的损伤过程。
