Minemori K, Nakajo S, Bamba T, Hosoda S
Second Department of Internal Medicine, Shiga University of Medical Science.
Nihon Shokakibyo Gakkai Zasshi. 1992 Feb;89(2):486-92.
To clarify the kinetics of cell membrane and intracellular mediators in the process of auranofin (AF)-induced diarrhea, we perfused electrolyte solution containing the oral gold preparation AF, which is a treatment for rheumatoid arthritis, through the rat jejunum, and studied net water and electrolyte transport, Na+, K(+)-ATPase activity, and c-AMP and c-GMP concentrations in the jejunal mucosa. In addition, change in Ca+ concentration in isolated intestinal cells was evaluated using fura-2-acetoxyl-methyl ester. AF significantly suppressed water and electrolyte transport. Mucosal secretion was increased due to elevation of the intracellular Ca+ concentration early in the perfusion period, then due to reduction in the Na+, K(+)-ATPase activity, and increase in the c-AMP concentration late in the perfusion period. Therefore, these cell membranes and intracellular mediators are considered to be involved in the mechanism of AF-induced diarrhea.
为了阐明金诺芬（AF）诱导腹泻过程中细胞膜和细胞内介质的动力学，我们将含有口服金制剂AF（一种用于治疗类风湿性关节炎的药物）的电解质溶液灌注通过大鼠空肠，并研究了空肠黏膜中的净水电解质转运、Na⁺、K⁺-ATP酶活性以及c-AMP和c-GMP浓度。此外，使用fura-2-乙酰氧基甲酯评估了分离的肠细胞中Ca⁺浓度的变化。AF显著抑制了水电解质转运。在灌注初期，由于细胞内Ca⁺浓度升高导致黏膜分泌增加，随后在灌注后期，由于Na⁺、K⁺-ATP酶活性降低以及c-AMP浓度增加导致黏膜分泌增加。因此，这些细胞膜和细胞内介质被认为参与了AF诱导腹泻的机制。
