Gvozdjáková A, Simko F, Kucharská J, Braunová Z, Psenek P, Kyselovic J
Pharmacobiochemical Laboratory of Medical Faculty, Comenius University, Bratislava, Slovak Republic.
Biofactors. 1999;10(1):61-5. doi: 10.1002/biof.5520100107.
The aim of the study was to show whether the ACE inhibitor captopril is able to protect the heart against the deleterious effect of passive cigarette smoking on left ventricular mitochondria. Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 minutes (S), control + captopril (7.5 mg/kg body weight twice daily) (Cap), and smoking + captopril (SCap) as in group 2 and 3. Three weeks lasting passive smoking impaired oxidative phosphorylation, diminished cytochrome oxidase activity and increased the mitochondrial F1-ATPase protein concentration. Moreover, the level of coenzyme Q10 (CoQ10) and coenzyme Q9 were decreased. Simultaneous treatment with captopril prevented partly the decrease of CoQ10 level, deterioration of oxidative phosphorylation, diminution of cytochrome oxidase activity and enhancement of F1-ATPase level. We conclude that captopril protected the myocardium against the harmful effect of passive smoking in rabbits.
该研究的目的是表明血管紧张素转换酶抑制剂卡托普利是否能够保护心脏免受被动吸烟对左心室线粒体的有害影响。对四组兔子进行了研究：对照组（C）、每天两次/30分钟被动吸三支烟（S）、对照组 + 卡托普利（每天两次，7.5毫克/千克体重）（Cap），以及如第2组和第3组那样的吸烟 + 卡托普利组（SCap）。持续三周的被动吸烟损害了氧化磷酸化，降低了细胞色素氧化酶活性，并增加了线粒体F1 - ATP酶蛋白浓度。此外，辅酶Q10（CoQ10）和辅酶Q9的水平降低。同时用卡托普利治疗部分预防了CoQ10水平的降低、氧化磷酸化的恶化、细胞色素氧化酶活性的降低以及F1 - ATP酶水平的升高。我们得出结论，卡托普利保护了兔心肌免受被动吸烟的有害影响。
