[The cardioprotective effect of perindopril in rats with experimental cardiosclerosis]. / Kardioprotektivnyi éffekt perindoprila u krys s éksperimental'nym kardiosklerozom.

Rats with experimental cardiosclerosis detected 21 days after embolization of the coronary arteries were subjected to early chronic perindopril administration (per os, 2 mg/kg once a day on days 2-20 after immobilization. As a result, the number of scars reduced, focal cardiosclerosis, dystrophy and hypertrophy of the cardiomyocytes were less pronounced, and the content of cellular glycogen increased. The cardioprotective effect was attended with a normalizing influence on the renin-angiotensin system parameters which were significantly changed after experimental damage to the myocardium: perindopril restored angiotensin I clearance and the level of angiotensin II production in the lungs.

Omega-3 fatty acid supplementation and lipoprotein(a) concentrations in patients with chronic glomerular diseases.

Renal disease patients often exhibit alterations in the lipid profile which may become an important risk of accelerated atherosclerosis and contribute to disease progression. Among such alterations, increased levels of lipoprotein(a) [Lp(a)] are common and may be related, in part, to the degree of proteinuria. Omega-3 polyunsaturated fatty acids (omega-3 FA) have been reported to decrease Lp(a) concentrations in nonrenal subjects. In addition, they have recently been shown to reduce proteinuria in patients with chronic glomerular disease. We therefore tested the hypothesis that omega-3 FA treatment in patients with chronic glomerular disease may reduce Lp(a) concentrations. Eight patients (2 with membranous glomerulonephritis, 6 with focal glomerular sclerosis) were submitted to a total of 13 six-week courses of treatment with omega-3 FA, at a dose of 3 g/day with a triglyceride preparation (n = 4) and of 7.7 g/day with an ethyl-ester preparation (n = 9). Both treatments significantly increased the proportions of omega-3 to omega-6 FA in total serum lipids, documenting compliance to treatment. Both treatments were also effective in decreasing serum thromboxane (from mean 490 +/- (SEM) 70 to 325 +/- 49 ng/ml, p < 0.05, in the high-dose group) and prolonging the bleeding time (from 5.8 +/- 0.4 to 7.7 +/- 0.5 min, p < 0.05, in the high-dose group), thus documenting the biological efficacy of treatment. However, despite a significant reduction in serum triglyceride levels (from 137 +/- 20 to 104 +/- 19 mg/dl in the high-dose group), Lp(a) concentrations did not change (292 +/- 120 U/l before, 315 +/- 130 U/l after the high-dose therapy). Treatment-related changes in proteinuria (from 2.9 +/- 0.5 to 2.1 +/- 0.7 g/24 h) were not related at all to changes in Lp(a) levels. We conclude that omega-3 FA do not decrease Lp(a) concentrations in renal patients with chronic glomerular diseases and that Lp(a) levels are unlikely to be related to the degree of proteinuria within the short-term modifications induced by omega-3 FA.