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Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.

To elucidate the effects of alcohol on thrombotic diseases we focussed on blood rheology which is one of the most important factors of blood flow. We measured the viscosity of whole blood and plasma of 18 healthy volunteers (11 males and 7 females) before and after drinking at a dinner party. There were significant increases in whole blood viscosity (7.4%, P less than 0.005) and plasma viscosity (3.0%, P less than 0.005) after drinking. Judging from the significant correlations between changes in blood viscosity and changes in variables related to hemoconcentration, the ability of alcohol to increase blood viscosity is considered to be due mainly to hemoconcentration. Alcohol itself did not increase whole blood viscosity in vitro at concentrations of 0.1, 0.2, 0.3 and 0.4% (w/v).

Eicosapentaenoic acid (EPA), which is abundant in seafood, has been reported to be a potent antagonist of platelet aggregation and also to reduce the incidene of cardiovascular disorders. We recently reported that EPA also reduces whole blood viscosity. A highly purified EPA, in a soft capsule (75% ethylester form of EPA; EPA-E), manufactured from sardine oil was administered to 8 healthy male subjects for 4 weeks. No side effects were observed. Platelet aggregation and platelet retention significantly decreased. The EPA content in platelet phospholipids markedly increased but docosahexaenoic acid (DHA) and arachidonic acid (AA) contents did not change. A reduction in whole blood viscosity and an increase in erythrocyte deformability were also observed after 4 week's ingestion of EPA-E. The EPA content in erythrocyte membrane phospholipids markedly increased after 4 weeks, and was positively correlated with erythrocyte deformability. Reduction of platelet aggregation and improvement of the rheological properties of the erythrocyte might be explained by an increase in the EPA content in platelet and erythrocyte phospholipids.