Koke J R, Shug A L, Folts J D, Bittar N
Cytobios. 1976;17(67-68):211-29.
The myocardial cellular response to the cardiac glycoside atractylate, a known inhibitor of mitochondrial adenine nucleotide translocation, was examined physiologically, morphologically, and morphometrically in eight dogs. An isolated in situ segment of left ventricular tissue was employed in these experiments to eliminate collateral flow and the potential for large sampling error. It was found that atractylate infusion rapidly induced physiological and morphological changes suggestive of a loss of membrane regulation of ion flux in the arteriole, capillary endothelium, and myocardial cell. Also mitochondrial changes suggestive of adenine nucleotide translocase inhibition were observed. As these responses are similar to those induced by acute myocardial ischaemia, it is suggested that ischaemia and atractylate induce cell injury by similar mechanisms.
在八只狗身上，从生理、形态和形态计量学方面研究了心肌细胞对强心苷白术内酯（一种已知的线粒体腺嘌呤核苷酸转运抑制剂）的反应。在这些实验中，采用左心室组织的原位分离段以消除侧支循环血流和较大抽样误差的可能性。结果发现，输注白术内酯迅速诱发了生理和形态学变化，提示小动脉、毛细血管内皮和心肌细胞的离子通量膜调节功能丧失。还观察到提示腺嘌呤核苷酸转位酶受抑制的线粒体变化。由于这些反应与急性心肌缺血诱发的反应相似，因此提示缺血和白术内酯通过相似的机制诱导细胞损伤。
