Journal of Nutrition

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


Journal of Nutrition Vol. 117 No. 9 September 1987, pp. 1520-1526
Copyright © 1987 by American Society for Nutrition
This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takahashi, R.
Right arrow Articles by Horrobin, D. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takahashi, R.
Right arrow Articles by Horrobin, D. F.

Impaired Platelet Aggregation and Thromboxane Generation in Essential Fatty Acid—Deficient Rats

Ryutaro Takahashi, Mehar S. Manku and David F. Horrobin

Efamol Research Institute, Kentville, Nova Scotia, Canada B4N 4H8

ADP-induced platelet aggregation and thrombin-induced thromboxane B2 generation in diluted whole blood from rats fed a fat-free diet supplemented with 10% (by weight) hydrogenated coconut oil [essential fatty acid (EFA) deficient] were significantly lower than that in animals fed 10% safflower oil [(SFO) rich in linoleic acid] or 10% marine oil (rich in eicosapentaenoic acid and docosahexaenoic acid). Plasma fibrinogen levels were significantly lower and liver function was impaired in the EFA-deficient group compared with the other two groups. Platelet responsiveness to ADP was restored when plasma from the EFA-deficient rats was replaced by plasma obtained from rats fed a nonpurified diet. ADP responsiveness and thrombin-stimulated thromboxane B2 production in diluted whole blood were also restored after 2 wk of injections of 100 mg ethyl linoleate every 48 h, and partially restored by injections of 100 mg ethyl {alpha}-linolenate. When ADP-induced platelet aggregation was examined in washed platelets, the impaired ADP aggregation (found when platelets of the EFA-deficient rats were suspended in their own plasma) was not observed at either high (9.5 µM) or low (1.0 µM) ADP concentrations. Although thrombin-stimulated thromboxane B2 production in washed platelets in the EFA-deficient rats was lower than that in the SFO-fed rats, the magnitude of aggregation was not different. In addition, inhibition of thrombin-induced platelet aggregation by apyrase (0.06 u/mL) was identical in the two groups. These results suggest that impaired platelet aggregation in EFA deficiency is related more to plasma factors than to inherent platelet properties and that restoration of normal liver function is associated with normal platelet function. Fibrinogen may play a role. The combined effects of reduced arachidonic acid composition in platelet phospholipids and impaired thrombin-ADP synergism in platelet aggregation seem to be responsible for the decreased thromboxane B2 production, but this may not be of major importance in impairing platelet function in EFA deficiency.


KEY WORDS: • platelet aggregation • thromboxane • fibrinogen • essential fatty acids • ADP

Manuscript received 17 November 1986. Revision accepted 15 May 1987.







Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]