Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Archives of Medical Science

Volume 4 - Number 8

Article Type: ---- Unspecified ----
Abstract:

Introduction: Metabolic acidosis is present in end stage renal disease. There is a link between enhanced endothelial permeability and accelerated atherosclerosis. In this study, we investigated the effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide (NO) concentration in normal and high-cholesterol fed rabbits. Material and methods: Twenty-four male rabbits were divided into four groups: normal, hypercholesterolemic, acidemic, and hypercholesterolemic plus acidemic. Acidosis and hypercholesterolemia were induced by drinking water containing ammonium chloride (NH4Cl), and cholesterol-rich animal chow (1%), respectively. After 6 weeks, blood samples were taken and endothelial permeability was measured using the Evans blue dye injection method. Results: Hypercholesterolemic animals had higher aortic endothelial permeability compared with normal groups (16.18 +/- 0.91 mu g EB/g tissue vs. 12.89 +/- 0.66 pg EB/g tissue, p < 0.05). Acidosis significantly increased endothelial permeability in the normal group (17.10 +/- 0.56 mu g/g tissue vs. 12.89 +/- 0.66 mu g/g tissue; p < 0.05) but did not further increase endothelial permeability in hypercholesterolemic animals (16.18 0.91 pg EB/g tissue vs. 17.29 +/- 0.46 mu g EB/g tissue; p > 0.05). Serum total cholesterol, low density lipoprotein (LDL) and NO concentrations in hypercholesterolemic animals were significantly higher than the normal group and acidosis could not change them either in the normal or in the high-cholesterol diet group. Conclusions: Alterations of serum lipids and NO are not the main mechanism for accelerated atherosclerosis during metabolic acidosis. Acidosis increases aortic endothelial permeability at least in a normal diet which may be a possible mechanism for progression of atherosclerosis processes in end-stage renal disease.

Keyword: