Evolution and involution of atherosclerosis and its relationship with vascular reactivity in hypercholesterolemic rabbits.
OBJECTIVE
The aim of this study is to verify the evolution and involution of experimental atherosclerosis in rabbits through the study of endothelial function, lipids and tissue lipid peroxidation, macro and microscopic quantification of aortic atherosclerosis.


METHODS
Thirty male New Zealand white rabbits were divided into six groups (n=5): G1 normal diet; G2: hypercholesterolemic receiving 0.5% of cholesterol diet for 4 months; G3: hypercholesterolemic diet for 4 months after normal diet for more 4 months; G4: hypercholesterolemic diet for 4 months plus normal diet and rosuvastatin for 1 month, G5: hypercholesterolemic diet for 4 months plus normal diet and rosuvastatin for 2 months, G6: hypercholesterolemic diet for 4 months plus normal diet and rosuvastatin for 4 months. Rosuvastatin was administered at a dosage of 5mg dissolved in 150 ml of water daily. At the end of the experiment were measured: total cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL-C), high density lipoprotein (HDL-C), tissue cholesterol (CAO), lipid peroxidation tissue (MDA). Endothelial function (RMAX) was studied in a segment of thoracic aorta, through curve-effect of acetylcholine and sodium nitroprusside. The amount of atherosclerosis was determined by measurement of the arterial lesion, through software, after staining with Sudan IV and histological staining.


RESULTS
In relation the water the rabbits drank 60-70 ml all day. It was seen significantly increase in all parameters at G2 both biochemical and tissue. In the group G3 it was seen significantly decrease in plasma lipids levels and tissue cholesterol. Treated groups G4, G5 and G6 all showed a decreased plasma lipid levels, only at G6 group it was noted a tissue cholesterol, tissue peroxidation and quantification of atherosclerosis, which showed a significant decrease. In relation the endothelial function only G6 improve significantly.


CONCLUSIONS
Our findings indicated that the treatment with rosuvastatin for 4 months is more efficient because improve the endothelial function significantly.
Laboratory of Endothelium, Lipids and Atherosclerosis, Center of Experimental Medicine and Surgery, Faculty of Medical Science, University of Campinas (UNICAMP), State of São Paulo, Brazil.
Michiko Regina
MR
Ozaki
Eros Antonio
EA
de Almeida
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D003627:Data Interpretation, Statistical; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D005464:Fluorobenzenes / Q000008:administration & dosage / Q000627:therapeutic use*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008055:Lipids / Q000097:blood; D008297:Male; D011743:Pyrimidines / Q000008:administration & dosage / Q000627:therapeutic use*; D011817:Rabbits; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000008:administration & dosage / Q000627:therapeutic use*; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects*
D002791:Cholesterol, Dietary; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium