Rapeseed Oil and Sunflower Oil Diets Enhance Platelet In Vitro Aggregation and Thromboxane Production in Healthy Men when Compared with Milk Fat or Habitual Diets

1992 ◽  
Vol 67 (03) ◽  
pp. 352-356 ◽  
Author(s):  
Marja Mutanen ◽  
Riitta Freese ◽  
Liisa M Valsta ◽  
Irma Ahola ◽  
Antti Ahlström
Keyword(s):  
Sunflower Oil ◽  
Milk Fat ◽  
Rapeseed Oil ◽  
Controlled Trial ◽  
Collagen Concentration ◽  
Aggregation Pattern ◽  
Thromboxane Production ◽  
Low Erucic Acid ◽  
Platelet Thromboxane

SummaryIn this highly controlled trial, 26 normolipidemic men (average age 28 years, range 18 to 60) were fed a baseline diet high in milk fat (MF) (fat 36% of energy, saturates 19%, monounsaturates 11%, polyunsaturates 4%), followed by a diet high in sunflower oil (SO) (fat 38% of energy, saturates 13%, monounsaturates 10%, polyunsaturates 13%) and another diet high in low erucic-acid rapeseed oil (RO) (fat 38% of energy, saturates 12%, monounsaturates 16%, polyunsaturates 8%). All diets were mixed natural diets with the same cholesterol contents. The baseline milk fat diet was given for 14 days and the oil diets for 24 days in a blind cross-over design. The platelet in vitro aggregation (slope %/min) induced by 1, 2 and 3 pM ADP and collagen (25 pg/ml PRP) was highly significantly (p <0.001) increased after both oil diets when compared with the results from the milk fat diet. The aggregation pattern determined by threshold collagen concentration confirmed increased collagen sensitivity of the platelets after the rapeseed oil diet (p <0.001). The enhancement of platelet aggregation was associated with increased in vitro platelet thromboxane production after the oil diets vs. the milk fat diet (p <0.05 after the sunflower oil diet and p <0.001 after the rapeseed oil diet).

scholarly journals Effects of milk fat, unhydrogenated and partially hydrogenated vegetable oils on fat metabolism of growing pigs: II. Changes in serum cholesterol and triglyceride levels

1993 ◽  
Vol 2 (1) ◽  
pp. 15-23
Author(s):  
Asmo Kemppinen ◽  
Matti Jauhiainen ◽  
Veikko Kankare ◽  
Jarmo Valaja ◽  
Timo Alaviuhkola ◽  
...  
Keyword(s):  
Serum Cholesterol ◽  
Sunflower Oil ◽  
Milk Fat ◽  
Rapeseed Oil ◽  
Fat Metabolism ◽  
Growing Pigs ◽  
Butter Oil ◽  
Gross Energy ◽  
Hydrogenated Vegetable Oils ◽  
Low Erucic Acid

Fifty mainly crossbred growing pigs were fed diets composed of a basal feed (2% fat) and supplemented 30% gross energy in the form of butter oil, cream, low erucic acid rapeseed oil (LEAR), sunflower oil or partially hydrogenated sunflower oil for 88 days in order to evaluate the effects of different food fats on their serum cholesterol and triglyceride levels. The levels of serum total cholesterol in the animals fed butter oil (3.47 mmol/l) and cream (3.48 mmol/l) were significantly (p

scholarly journals Effect of diet supplementation with sunflower oil on milk production, fatty acid profile and ruminal fermentation in lactating dairy ewes

2008 ◽  
Vol 75 (4) ◽  
pp. 399-405 ◽  
Author(s):  
Gonzalo Hervás ◽  
Pilar Luna ◽  
Ángel R. Mantecón ◽  
Natalia Castañares ◽  
Miguel Angel de la Fuente ◽  
...  
Keyword(s):  
Milk Production ◽  
Sunflower Oil ◽  
Milk Fat ◽  
Total Solid ◽  
Ruminal Fermentation ◽  
Fat Percentage ◽  
Negative Effects ◽  
Rumen Microorganisms ◽  
Diet Supplementation

The aim of this research was to enhance the nutritional quality of ewe milk fat by increasing potentially healthy fatty acids (FA) through diet supplementation with unprotected oil rich in linoleic acid, and without detrimental effects on animal performance. Twenty-four ewes were assigned to two high concentrate diets, control or supplemented with 6% sunflower oil (SO), for 4 weeks. No differences between treatments were found in milk production and dry matter intake. Although the SO diet increased milk fat percentage and tended to reduce milk protein concentration, it did not affect milk fat, protein or total solid yield. Most of the modifications in milk FA composition were addressed toward a potentially healthier profile: a decrease in C12:0 to C16:0 and a remarkable increase in the contents of cis-9 trans-11 C18:2 (from 0·94 to 3·60 g/100 g total FA) and trans-11 C18:1 (from 2·23 to 8·61 g/100 g total FA). Furthermore, the levels reached were maintained throughout the period monitored. However, the SO diet increased other trans C18:1 isomer percentages, too. The lack of differences between treatments in the in vitro ruminal fermentation parameters, studied with batch cultures of rumen microorganisms, would indicate no negative effects on ruminal fermentation.

NIACIN-INDUCED PROSTACYCLIN (PGI2) GENERATION AND THE SEARCH FOR THE IDEAL DOSE OF ASPIRIN

1987 ◽  
Author(s):  
J A Jakubowski ◽  
D Deykin
Keyword(s):  
Plasma Levels ◽  
Chronic Administration ◽  
Normal Subjects ◽  
Enteric Coated Aspirin ◽  
Regular Aspirin ◽  
Thromboxane Production ◽  
Enteric Coated ◽  
Platelet Thromboxane

We have previously reported that chronic administration of 80 mg/day of enteric-coated aspirin (ECA) in three divided doses of 27 mg each day for 7 days produced over 90% inhibition of platelet thromboxane production. What we wanted to know was whether that dose of aspirin spared PGI2 production. We developed a sensitive plasma assay for PGI2 (measured as 6-keto-PGF1a). We confirmed the reports of others that normal plasma levels are very low, less than 2 pg/ml. We selected niacin as a provocative challenge to raise plasma levels of PGI2 to test the ability of a given aspirin regimen to spare or suppress PGI2 production in vivo. In 5 normal subjects an oral dose of 3 mg/kg of niacin produced a 3-fold rise in 6-keto-PGF1a from 0.86 to 2.64 pg/ml. A dose of 5 mg/kg produced a rise to 6.6 pg/ml. Administration of 323 mg of regular aspirin/day for 7 days completely abolished niacin-induced elevation of plasma PGI2. The lowest dose of ECA that we have found effective in suppressing platelet thromboxane production in vitro, 80 mg/day in divided doses of 27 mg three times a day for 7 days, also completely suppressed niacin-induced elevation of PGI2. Our data do not support the hyypothesis that a very low dose of ECA selectively suppress platelet thromboxane production but spares generation of PGI2

In Vitro Effects Of 5-Fluorouracil On Vascular Tissue Prostacyclin Release And Platelet Thromboxane Production

1981 ◽  
Author(s):  
L Caprino ◽  
F Antonetti ◽  
M Lagomarsino ◽  
L Morelli
Keyword(s):  
Platelet Aggregation ◽  
Vascular Tissue ◽  
Wet Weight ◽  
Thromboxane Production ◽  
In Vitro Effects ◽  
Dose Levels ◽  
Dose Dependent Increase ◽  
Platelet Thromboxane

Severe chest pain (angina attacks) and myocardial infarction has been recorded during 5-Fluorouracil (5-F.U.) tre atment. The present study was undertaken to evaluate the "in vitro" activity of 5-F.U. on vascular prostacyclin (PGI ) release and platelet thromboxane A2(TXA2) formation, which play a role in the onset of cardiovascular disorders. Rat aortic rings (about 20 mg wet/weight) were incubated at 30*C for 15 mins in 300 pi tris buffer containing 5-F.U. (250-500-1000 yg). The aortic rings were removed and the supernatant was kept 4 hrs at room temperature and the RIA of 6-keto PGF1α was thereafter performed.In 1 ml rabbit PRP containing 5-F.U. (50-100-500 yg) platelet aggregation was induced by Arachidonic acid (45 μg). Platelets were then removed by centrifugation and RIA of TXB2 was performed on supernatant.At the dose levels of 250, 500, 1000 μg, 5-F.U. yielded a dose-dependent increase (20, 44 and 68 percent, respectively) in the 6-keto PGF2 released by rat aortic rings. Coil versely, the TXB2 production by platelets during aggregation was reduced of 19, 27, 36 percent at 5-F.U. concentrations of 50, 100, 500 μg/ml, respectively. 5-F.U. had no effect on platelet aggregation.Considering the vasodilator and antithrombogenic effects of PGI2 and the vasoconstrictor effect of TXA2 the present results are not in agreement with the already described cardiotoxicity of 5-F.U. The “in vitro” results, however, if confirmed “in vivo”, show a new aspect of the mechanism of 5-F.U. cardiotoxicity.

Comparison of the Effects of Two Diets Rich in Monounsaturated Fatty Acids Differing in their Linoleic/α-Linolenic Acid Ratio on Platelet Aggregation

1994 ◽  
Vol 71 (01) ◽  
pp. 073-077 ◽  
Author(s):  
Riitta Freese ◽  
Marja Mutanen ◽  
Liisa M Valsta ◽  
Irma Salminen
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Platelet Aggregation ◽  
Linolenic Acid ◽  
Sunflower Oil ◽  
Rapeseed Oil ◽  
Monounsaturated Fatty Acids ◽  
Acid Ratio ◽  
Induced Aggregation

SummaryThe effect of dietary linoleic/α-linolenic acid ratio on human platelet aggregation in vitro was investigated using low-erucic acid rapeseed oil and high-oleic acid sunflower oil as the major fat sources. In a cross-over study 20 healthy male subjects, average age 29 year (range 20–46 yr), followed experimental rapeseed oil (RO) and Trisun-sunflower oil (TSO) diets after their habitual diet for six weeks. Subjects were provided most of the fat containing foods but were allowed to eat other foods almost freely. Fatty acid compositions of the diets calculated from dietary records were as follows (saturated/monounsaturated/polyunsaturated fatty acids): RO diet 12.4/18.6/8.9% of total energy (en%) (linoleic/α-linolenic acid ratio 2.8) and TSO diet 11.8/17.8/8.3 en% (linoleic/α-linolenic acid ratio 28), respectively. Plasma cholesterol ester fatty acid composition proved compliance to the experimental diets. Platelet aggregations induced by ADP (1,2 and 3 μM) or thrombin (0.12, 0.15 and 0.18 NIH/ml) were significantly enhanced and collagen- (1.5, 2.5 and 5.0 μg/ml) induced aggregation tended to be enhanced after the TSO diet compared with the RO diet. After the TSO diet platelet aggregation was enhanced from the level of the habitual diets by one thrombin (0.18 NIH/ml), one collagen (1.5 μg/ml) and all three ADP concentrations. The diets had no effect on antithrombin III activity. Results show that platelet aggregation in vitro decreases as the ratio of linoleic acid to a-linolenic acid decreases in diets rich in monounsaturated fatty acids.

The Effect of Endralazine and Hydralazine on Platelet Thromboxane Production in Vitro

1987 ◽  
Vol 6 (3) ◽  
pp. 375-386
Author(s):  
I. A. Greer ◽  
J. J. Walker ◽  
M. McLaren ◽  
A. A. Calder ◽  
C. D. Forbes
Keyword(s):  
Thromboxane Production ◽  
Platelet Thromboxane

The Interrelationship between Thromboxane Biosynthesis, Aggregation and 5-Hydroxytryptamine Secretion in Human Platelets in Vitro

1980 ◽  
Vol 43 (01) ◽  
pp. 038-040 ◽  
Author(s):  
L C Best ◽  
T K Holland ◽  
P B B Jones ◽  
R G G Russell
Keyword(s):  
Human Platelet ◽  
Human Platelets ◽  
Dense Granule ◽  
Thromboxane B2 ◽  
Essential Requirement ◽  
Direct Mechanism ◽  
Thromboxane Synthetase ◽  
Thromboxane Production ◽  
Higher Doses

SummaryPlatelet aggregation, secretion of 5-hydroxy tryptamine and production of thromboxane B2 were monitored simultaneously in human platelet suspensions in the absence and presence of cyclooxygenase or thromboxane synthetase inhibitors. Aggregation, secretion and thromboxane B2 formation in response to either sodium arachidonate or epinephrine were blocked by aspirin or by 1-N-butyl imidazole suggesting that thromboxane biosynthesis was an essential requirement for platelet activation by these agents. In contrast, thrombin and collagen could apparently induce aggregation and secretion via two pathways: at low doses involving thromboxane production, but at higher doses by a direct mechanism independent of thromboxane biosynthesis. In the case of ADP, inhibition of thromboxane production blocked secretion but had little effect on aggregation, indicating that secretion was probably dependent on thromboxane biosynthesis which probably occurred as a result of aggregation. Thus it appears that although the processes of thromboxane production, release of dense granule constituents and aggregation may often be intimately linked, each process can occur independently of the other, depending upon the stimulus used.

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