[Effects of atorvastatin and CoQ(10) on myocardial energy metabolism in rabbits with hypercholesterolemia].

OBJECTIVE: To explore the interventional effects of atorvastatin and CoQ(10) on myocardial energy metabolism in rabbits with hypercholesterolemia. METHODS: Forty male New Zealand white rabbits were randomly divided into 5 groups: i.e. normal control, high cholesterol, statin, coenzyme Q(10) 1 and coenzyme Q(10) 2. After feeding for 6 weeks, the fasting blood samples were collected through ear marginal vein and the serum level of total cholesterol was determined. Myocardium was sampled for ultrastructures by electron microscopy; high-performance liquid chromatography (HPLC) was used to measure myocardial mitochondria adenosine triphosphate (ATP) and coenzyme CoQ(10). Ultraviolet spectrophotometry was used to measure the activities of mitochondrial complexes II and IV. RESULTS: In high cholesterol group, myocardial fibers were arrayed disorderly with partial rupture and dissolution. There was mitochondrial swelling with disorderly and fuzzy cristae. As compared with the controls, the activities of mitochondrial respiratory chain complexes II and IV declined (5.39 ± 0.53 vs 12.95 ± 0.99, 1.89 ± 0.26 vs 6.65 ± 0.95, P < 0.01), the contents of mitochondrial ATP and CoQ(10) decreased (0.17 ± 0.05 vs 0.44 ± 0.06, 0.09 ± 0.02 vs 0.25 ± 0.04, P < 0.01); for statin group versus high cholesterol group, the activities of mitochondrial respiratory chain complexes II and IV increased (9.12 ± 1.19 vs 5.39 ± 0.53, 4.61 ± 0.52 vs 1.89 ± 0.26, P < 0.01); the content differences of mitochondrial ATP and CoQ(10) were statistically insignificant. For CoQ(10) 1 group versus statin group, the differences of respiratory chain complexes II and IV were statistically insignificant; the contents of mitochondria ATP and CoQ(10) increased (0.35 ± 0.03 vs 0.16 ± 0.04, 0.17 ± 0.02 vs 0.07 ± 0.02, P < 0.01). For coenzyme Q(10) 2 group versus coenzyme Q(10) 1 group, none of the indices was statistically significant. CONCLUSION: High cholesterol can cause myocardial ultrastructural changes and impaired mitochondrial energy metabolism. Atorvastatin reduces the myocardial structural damage and the combination of atorvastatin and CoQ(10) may further improve the myocardial mitochondrial energy metabolism.

[The effect of captopril and valsartan on preventing the formation of atherosclerotic plaque].

OBJECTIVE: To observe the effect of captopril and valsartan on preventing the formation of atherosclerosis plaque in rabbit atherosclerotic models. METHODS: The atherosclerotic models of rabbits fed with high-cholesterol diet were used. There were four groups: high cholesterol group, high cholesterol + captopril group, high cholesterol + valsartan group, normal food group. The intima-media thickness in abdominal aortic were measured by ultrasound. The pathogenic features of the arterial walls were showed by HE stain and observed by light microscope. RESULTS: There were less atherosclerotic plaque in high cholesterol + captopril group and high cholesterol + valsartan group than in cholesterol group. The intima-media thickness in high cholesterol + captopril group and in high cholesterol + valsartan group were much more decreased than in high cholesterol group (0.05 +/- 0.005, 0.05 +/- 0.007 vs 0.07 +/- 0.100, P < 0.01). The connection of the endothelial cells were less damaged in high cholesterol + captopril group and high cholesterol + valsartan group than in high cholesterol group. CONCLUSIONS: Ti is true that angiotensin converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) have the effect of preventing or decreasing the formation of atherosclerotic plaque in arterial wall. The findings suggest that ACEI and/or ARB should be first chosen for those with hypertension and with atherosclerotic risk factors or atherosclerotic diseases.