Myocardial lipidosis

Myocardial fat infiltration in the rat heart is directly related to long chain monoenoic fatty acids with 20 or more carbon atoms. The docosenoic (22 1) fatty acids are more damaging than the eicosenoic (20 1) fatty acids (Beare-Rogers eta/., 1972a). Presumably, the tetracosenoic (24 1) fatty acids would be even more effective in producing myocardial lipidosis, although this has not been tested experimentally. 

Myocardial Lipidosis Caused by Different Docosenoic Fatty Acids... 

A grading system was used in which increasing number of pluses represents increasing severity of myocardial lipidosis. 

Myocardial lipidosis develops in both male and female albino rats when fed diets which contain the same quantity of docosenolc fatty acids (Beare-Rogers eta/., 1971 Kramer eta/., 1973). It has been suggested that lipidosis disappears slightly more rapidly in female rats than in male rats (Engfeldt and Brunius, 1975b). 

On the other hand, myocardial necrosis occurs in male rats even in the absence of myocardial lipidosis. Kramer et a/. (1973) observed that when male rats were fed a diet that contained either lard, corn oil, or a low erucic acid rapeseed oil, either no, or very little myocardial lipidosis developed, but still the rats showed myocardial necrosis after 16 weeks on test. This indicates that myocardial necrosis can develop independently of the early myocardial fat accumulation. 

Comparison of Myocardial Lipidosis in Pigs and Rats as Determined Histologically by Oil Red O Staining ... 

The occurrence of myocardial lipidosis in piglets fed diets that contain HEAR oil is by no means a consistent finding. Canadian scientists have shown that in pigs fed a diet containing 15% HEAR oil with an erucic acid content of 21%, there was no histological evidence of lipidosis, and there were not any dietary related lesions in muscle, liver, or spleen (Aherne et a/., 1975). A second study reported a year later by the same group with a HEAR oil of 34% erucic acid also failed to show evidence of myocardial lipidosis (Aherne et a/., 1976). 

Because the rat is highly susceptible to myocardial lipidosis when fed diets that contain 22 1, some health regulatory agencies deemed it prudent to limit the content of these acids in the human diet. 

Abdellatif and Vies (1970a) using frozen sections stained with Sudan red were the first to describe the presence of intracellular fat globules in the myocardium, skeletal muscles, and adrenals of rats fed HEAR oil. These workers noted pale hearts, skeletal muscles, and adrenals in rats fed HEAR oil but not in control animals fed sunflower oil. The myocardial lipidosis in the rats fed HEAR oil was present after 1 day of feeding, reached a peak at 6 days, was greatly diminished at 4 and 8 weeks, and had almost disappeared after 16 weeks. The feeding of glyceryl trierucate to rats produced a similar lipidosis. 

An electron microscopic study of the early stages of myocardial lipidosis... 

Ratanasethkul et al. (1976) fed chickens, ducks, and turkeys high and low erucic acid rapeseed oil, soybean oil, and a lard/corn oil control diet. All the ducks and some of the chickens fed the HEAR oil diet (36% erucic acid) died with hydropericardium and ascites. Myocardial lipidosis was present in all species fed the HEAR oil and the severity of the lipidosis (as judged by oil red O staining) decreased with time on diet. In ducks, they found thickening of the epicardium and myocardial fibrosis. Granulomas characterized by giant cells and histiocytic infiltration were present in some of the hearts of turkeys fed the HEAR oil. 

Myocardial lipidosis is produced in the rat by feeding various marine and rapeseed oils. This lipidosis reaches a peak at 6-7 days and declines thereafter. The severity and duration of this lesion are directly related to the docosenoic acid content of the diet. 

Poultry when fed high erucic acid rapeseed oils develop myocardial lipidosis, myocardial degeneration, hydropericardium and ascites. The occurrence and severity of these lesions would appear to be related to the amount of erucic acid in the diet. 

Perhaps equally as challenging as the question of why erucic acid causes myocardial lipidosis is the question of why the myocardial lipidosis abates and almost disappears even when experimental animals are maintained on exactly the same erucic acid containing diet that caused the lipidosis in the first place. 

---