Lönnrot K, Tolvanen J P, Pörsti I, Ahola T, Hervonen A, Alho H
Laboratory of Neurobiology, University of Tampere, Medical School, Finland.
Life Sci. 1999;64(5):315-23. doi: 10.1016/s0024-3205(98)00567-0.
Many studies have suggested that parenteral administration of coenzyme Q10 (Q10) protects the myocardium of young experimental animals from post-ischemic reperfusion injury. Although parenteral administration, in contrast to per os supplementation, seems to elevate coenzyme Q concentrations in heart tissue, it is not suitable for prophylactic use. In addition, the incidence of ischemic events is greatest in older age. We studied the effect of Q10 supplementation on myocardial postischemic recovery in 18-month-old Wistar rats. The treated group (n=9) received 10 mg/kg/day of Q10 for 8 weeks in their chow while the normal chow of the control group (n=9) contained less than 0.5 mg/kg/day of Q10. The treatment clearly elevated plasma Q10 concentration (286 +/- 25 micromol/l and 48 +/- 30 micromol/l, treated and controls, respectively, p<0.0001) but neither Q9 nor Q10 concentrations in heart tissue were affected by the supplementation. The isolated perfused hearts were subjected to 20 minutes of ischemia and 30 minutes of reperfusion. The preischemic values of developed pressure (DP) but not contractility (+DP/delta t) and relaxation (-DP/delta t) were improved by Q10 supplementation (p=0.034, p=0.057 and p=0.13, respectively) while in postischemic recovery no differences were observed between the groups (p>0.05 at all time points). Also, in myocardial flow, myocardial oxygen consumption (MVO2) and myocardial aerobic efficiency (DP/MVO2) the groups did not differ at any time points. Although dietary Q10 supplementation clearly elevated plasma Q10 concentrations in senescent rats, the coenzyme Q contents in heart tissue and myocardial recovery from ischemia were not affected. However, it is possible that the site of action for the reported beneficial effects of Q10 is in the coronary endothelium rather than myocardium itself.
许多研究表明,肠胃外给予辅酶Q10(Q10)可保护幼年实验动物的心肌免受缺血后再灌注损伤。尽管与口服补充相比,肠胃外给药似乎能提高心脏组织中的辅酶Q浓度,但它并不适合预防性使用。此外,缺血事件的发生率在老年时最高。我们研究了补充Q10对18月龄Wistar大鼠心肌缺血后恢复的影响。治疗组(n = 9)在其食物中连续8周每天给予10 mg/kg的Q10,而对照组(n = 9)的正常食物中Q10含量低于0.5 mg/kg/天。该治疗明显提高了血浆Q10浓度(治疗组和对照组分别为286±25 μmol/L和48±30 μmol/L,p<0.0001),但补充Q10对心脏组织中的Q9和Q10浓度均无影响。分离的灌注心脏经历20分钟的缺血和30分钟的再灌注。补充Q10改善了缺血前的舒张末压力(DP)值,但对收缩性(+DP/Δt)和舒张(-DP/Δt)无影响(分别为p = 0.034、p = 0.057和p = 0.13),而在缺血后恢复过程中,两组之间未观察到差异(所有时间点p>0.05)。此外,在心肌血流量、心肌耗氧量(MVO2)和心肌有氧效率(DP/MVO2)方面,两组在任何时间点均无差异。尽管饮食中补充Q10明显提高了衰老大鼠的血浆Q10浓度,但心脏组织中的辅酶Q含量和心肌缺血后的恢复并未受到影响。然而,Q10所报道的有益作用的作用位点可能在冠状动脉内皮而非心肌本身。