1975 Volume 2 Issue 4 Pages 257-266
It is well known that risk factors of atherosclerosis, such as hypertention, stress or hyperlipidemia, provoke the increase of vascular permeability to accumulate lipid in arterial wall. In fact, one shot treatment of angiotensin II, adrenaline, cholestrol or cigarett smoking induced experimentally edematous change in the aortic wall of experimental animals. In this studies, induction of atherosclerotic change in aortic wall of rabbits by repeated challenge with these risk factors were pursued histochemically and microbiochemically.
4 groups of rabbits were respectively challenged every day with 1γ/kg of angiotensin II (IV), 1g/kg of cholestrol (PO), 1% cholestrol containing diet feeding (150g/day) or 1cc of saline (IV) or 10cc of saline through gastric tube as a placebo control for 2 weeks or 4 weeks.
In 2 weeks' treated rabbits, histological study revealed commonly the intimal change in the aortic wall of rabbits challenged with cholestrol or angiotensin characterized with cell proliferation and a scanty of lipid accumulation.
A decrease of PR, ATPase, a slight increase of acid pase, esterase and lipase activities were observed in the aortic wall of rabbits in all three groups, compared with those in placebo control rabbits.
Microbiochemical assay of phosphofructokinase by Lowry's method modefied by us exhibited an increased activity in intima of all three groups. Especially statistically significant increase was certified in intima of cholestrol challenged groups.
In 4 weeks treatment, foam cells began to appear in intima of both cholestrol challenged groups and lipase, esterase and G-6PDH activities became striking in media of these group.
On the contrary, the decreased glycolytic enzyme activities such as PR, LDH, PFK, or MDH were remarkable in the middle part of media of the rabbits treated with angiotensin.
A statistically significant decrease in the activity of PFK in this lesion was a found microbiochemically (P<0.05).
These studies suggest that repeated challenges with one shot treatment of risk factors, such as epinephrine, angiotensin or cholestrol give commonly rise to intimal thickening characterized with cell proliferation and that further continuous challenges forces them to atherosclerotic change characterized with the quality of risk factors.
