Display options
Share it on
Full text links
Silverchair Information Systems

Eur Heart J. 1989 Sep;10(9):838-46. doi: 10.1093/oxfordjournals.eurheartj.a059579.

Mackerel oil and atherosclerosis in pigs.

European heart journal

L M Sassen, J M Hartog, J M Lamers, M Klompe, L J Van Woerkens, P D Verdouw

Affiliations

  1. Laboratory for Experimental Cardiology (Thoraxcenter), Erasmus University, Rotterdam, The Netherlands.

PMID: 2806283 DOI: 10.1093/oxfordjournals.eurheartj.a059579

Abstract

In 35 pigs atherosclerosis was induced by balloon abrasion and a diet containing 2% (w/w) cholesterol and 7% (w/w) lard fat. After 4 months of induction nine animals were killed (I) for analysis of the extent of atherosclerosis, while the diet of the other 26 pigs was changed to a low cholesterol diet containing either 9% (w/w) lard fat (L), 9% (w/w) fish oil (F) or 4.5% (w/w) lard fat and 4.5% (w/w) fish oil (LF). This diet was continued for 3 months to induce regression of atherosclerosis. The cholesterol-rich diet increased plasma total cholesterol, but did not affect plasma triglycerides. Low-cholesterol feeding decreased plasma total cholesterol in all three groups, but triglycerides only in LF and F. Lipid infiltration of the aortic wall was similar in I, L, LF and F. In the denudated coronary arteries of I mean luminal encroachment was 11 +/- 2%. This was similar in L (13 +/- 4%) but significantly lower (P less than 0.05) in LF (6 +/- 2%) and in F (3 +/- 1%). In the non-abraded coronary arteries of I mean luminal encroachment was 1.3 +/- 0.3%. For F and LF similar values were found, but in L there was an increase to 11 +/- 3% during low-cholesterol feeding. ADP-induced platelet aggregation was lower in LF and F than in L. Thromboxane A2 production was only reduced in F, while the production of the weak thromboxane A3 agonist was larger in F than in LF. It is concluded that fish oil retards the progression of and causes regression of coronary atherosclerosis.

Similar articles

Laurance WF.
Trends Ecol Evol. 2000 Sep;15(9):373. doi: 10.1016/s0169-5347(00)01916-9.
PMID: 10931671

Cited by

Substances

MeSH terms

Publication Types

LinkOut - more resources