Liu M S, Spitzer J J
Circ Shock. 1977;4(2):181-90.
We studied the in vitro effect of E. coli endotoxin on the oxidation of palmitate, palmitoyl CoA, and lactate by canine heart homogenate. Heart homogenates were incubated in calcium-free Krebs-Ringer-phosphate buffer in the presence of a 14C-labeled substrate. Oxidation of the individual substrate was calculated from the rate of 14CO2 production. The rate of oxidation of palmitate, palmitoyl CoA, and lactate was proportionally inhibited by increasing amounts (80-800 microgram) of endotoxin. The decrease in substrate oxidation could be mimicked by adding calcium chloride to the tissue preparation, and could be effectively prevented by the chelating agent, EDTA. Ionic calcium was released from tissue stores during incubation of the tissue preparation with endotoxin. These findings demonstrate that E. coli endotoxin inhibits substrate oxidation by heart homogenates when incubated under in vitro conditions. The data also suggest that the inhibition may be mediated by ionic calcium released from the tissue in response to the action of endotoxin.
我们研究了大肠杆菌内毒素对犬心脏匀浆中棕榈酸、棕榈酰辅酶A和乳酸氧化的体外作用。心脏匀浆在无钙的 Krebs-Ringer-磷酸盐缓冲液中，于一种14C标记的底物存在的情况下进行孵育。根据14CO2的生成速率计算各底物的氧化速率。随着内毒素量（80 - 800微克）的增加，棕榈酸、棕榈酰辅酶A和乳酸的氧化速率受到成比例的抑制。通过向组织制剂中添加氯化钙可模拟底物氧化的降低，而螯合剂乙二胺四乙酸（EDTA）可有效防止这种情况。在组织制剂与内毒素孵育期间，离子钙从组织储存中释放出来。这些发现表明，在体外条件下孵育时，大肠杆菌内毒素会抑制心脏匀浆的底物氧化。数据还表明，这种抑制作用可能是由组织因内毒素作用而释放的离子钙介导的。
