Dietary Supplementation with Low-Dose Fish Oils Lowers Fibrinogen Levels: A Randomized, Double-Blind Controlled Study

Radack, Kenneth L.; Deck, Colleen; Huster, Gertrude A.

doi:10.7326/0003-4819-111-9-757

Cited by 78 publications

(17 citation statements)

References 8 publications

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“…This observation does not support the assumption that changes in microhemodynamic or -rheologic conditions may have contributed to the observed effects of fish oil diet on postischemic leukocyte adhesion. How far the reduction of plasma fibrinogen observed in the fish oil-fed hamsters in our study (Table 3) and by others (38) contributes to the reduction of ischemia-reperfusion injury is not clear but deserves further study, in particular since fibrinogen has been shown to bind to the CD11b/CD18 adherence receptor on leukocytes (39).…”

Section: Discussionmentioning

confidence: 70%

Dietary fish oil blocks the microcirculatory manifestations of ischemia-reperfusion injury in striated muscle in hamsters.

Lehr

Hübner

Nölte

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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Epidemiologic observations and experimental studies have demonstrated a protective effect of dietary fish oil on the clinical manifestations of ischemia-reperfusion injury. To investigate the underlying mechanisms, we used the dorsal skinfold chamber model for intravital fluorescence microscopy of the microcirculation in striated muscle of awake hamsters. In control hamsters (n = 7), reperfusion after a 4-hr pressure-induced ischemia to the muscle tissue elicited the adhesion of fluorescently stained leukocytes to the endothelium of postcapillary venules, capillary obstruction, and the breakdown of endothelial integrity. These microvascular manifestations of ischemia-reperfusion injury were significandy attenuated in animals (n = 7) when fed with a fish oil-enriched diet for 4 weeks prior to the experiments. In leukocyte total lipids, the fish oil diet resulted in a substantial displacement of arachidonic acid, the precursor of the potent adhesionpromoting leukotriene (LT) B4, by fish oil-derived eicosapentaenoic acid, the precursor of biologically less potent LTBS, emphasizing the mediator role of LTB4 in ischemiareperfusion injury. These results suggest that the preservation of microvascular perfusion by dietary fish oil contributes to its protective effects on the clinical manifestations of ischemiareperfusion injury.Epidemiologic observations in Greenland Eskimos (1) and large prospective studies on Dutch (2) and American (United States) subjects (3) have shown that a high dietary intake of n-3 fatty acids, the predominant fatty acids in fish and fish oil, correlates with a low mortality from myocardial infarction. Although the underlying mechanism has not been fully elucidated, there is evidence that fish oil diet exerts a protective effect on the manifestation of ischemia-reperfusion injury in models of experimental myocardial and cerebral ischemia (4-6).The manifestations of ischemia-reperfusion injury are characterized by the chemotactic accumulation, aggregation, and adhesion of circulating leukocytes to the microvascular endothelium (7). Through the plugging of capillaries and the release of toxic degranulation products and oxygen metabolites, adherent leukocytes contribute to the final extent of ischemia-reperfusion injury, characterized by the breakdown of capillary perfusion (8) and the loss of endothelial integrity (9). The central role of leukocyte adhesion in the pathophysiologic sequelae of ischemia-reperfusion injury has been inferred from experiments where ischemiareperfusion injury was significantly reduced by neutrophil depletion with anti-neutrophil serum (7) or by monoclonal antibodies blocking leukocyte adhesion receptors (7, 10).The microcirculatory manifestations of ischemiareperfusion injury are similar to the microcirculatory changes brought about by the actions of leukotrienes (LTs), metabolites of arachidonic acid (20:4, AA) produced in the 5-lipoxygenase pathway. The dihydroxylated LTB4 has been shown to elicit leukocyte accumulation and adhesion to the endothelial lining (...

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Section: Discussionmentioning

confidence: 70%

Dietary fish oil blocks the microcirculatory manifestations of ischemia-reperfusion injury in striated muscle in hamsters.

Lehr

Hübner

Nölte

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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“…In parallel with the ability to affect plasma fibrinogen levels [8][9][10], prolonged administration of N-3 fatty acids is associated with the impairment of several monocyte functions, including the synthesis of TNF, IL-1, PAF, and leukotrienes [11,12]. The low plasma fibrinogen levels of chronic alcohol drinkers [13,14] are associated with changes in major functions of monocytes [15].…”

Section: Factors Affecting Plasma Fibrinogen Levelsmentioning

confidence: 99%

Drugs affecting plasma fibrinogen levels

Minno¹,

Mancini²

1992

Cardiovasc Drug Ther

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Current knowledge indicates that high plasma levels of fibrinogen help predict stroke and myocardial infarction. It is known that plasma fibrinogen is synthesized in the liver, that interleukin-6 (IL-6) affects this synthesis, and that, when exposed to appropriate stimuli, monocytes generate a variety of monokines, including IL-6. It is also known that prolonged administration of N-3 fatty acids, ticlopidine, fibrates, pentoxifylline, or alcohol lower plasma fibrinogen levels. The mechanism(s) involved in this effect are poorly understood. However, in view of the role of IL-6 and monocytes in the regulation of plasma fibrinogen levels, it is conceivable that the lowering effect of these drugs involves effects on some steps of the regulatory machinery. In addition to fibrinogen, IL-6 regulates the synthesis of other acute-phase proteins. This raises the question of whether high plasma fibrinogen levels do reflect the response of an acute-phase reactant to the severity of the atherosclerotic vascular damage taking place. Current evidence is inconclusive with respect to this possibility. On the other hand, the epidemiological data available indicate that measurements of plasma fibrinogen should be included in the cardiovascular risk-factor profile. In view of this, we believe that information emerging from population-based studies in which plasma fibrinogen is measured is important to identify appropriate directions to be followed to address unsolved issues in the area.

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“…EPA reduces fibrinogen levels and decreases whole blood viscosity [61, 62] as well as inhibits platelet functions. Black tree fungus, a common component of Chinese foods, is also purported to have platelet-inhibiting functions.…”

Section: What Antiplatelet Agents Are Now Used?mentioning

confidence: 99%

Antiplatelet Therapy in Stroke Prevention: Present and Future

Caplan¹

2006

Cerebrovasc Dis

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White platelet-fibrin thrombi often form on roughened endothelial surfaces and unstable arterial plaques. Agents that reduce the tendency of platelets to aggregate, agglutinate, and secrete and to attach to endothelial surfaces have been explored as agents that prevent brain and heart infarction. Aspirin, ticlopidine, clopidogrel, dipyridamole, cilostazol, and glycoprotein llb/llla inhibitors are all used now and have various different modes of action and functions.

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Dietary Supplementation with Low-Dose Fish Oils Lowers Fibrinogen Levels: A Randomized, Double-Blind Controlled Study

Cited by 78 publications

References 8 publications

Dietary fish oil blocks the microcirculatory manifestations of ischemia-reperfusion injury in striated muscle in hamsters.

Dietary fish oil blocks the microcirculatory manifestations of ischemia-reperfusion injury in striated muscle in hamsters.

Drugs affecting plasma fibrinogen levels

Antiplatelet Therapy in Stroke Prevention: Present and Future

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