Acetylsalicylic acid inhibits aggregation of blood platelets through affecting arachidon acid metabolism - a precursor of thromboxan which is a strong platelet aggregation inhibitor. A standard method for measurement of aggregation activity blockade (in percents) of platelet rich plasma is turbidimetric aggregomethry based on spectrophotometric principle. According to results of recent studies administration of acetylsalicylic acid is one of the basic pillars of prevention of thrombotic complications in atherosclerotic arterial disease. Acetylsalicylic acid doses differ from study to study. An aim of our work was to measure speed of two different doses of acetylsalicylic acid. Results: Level of aggregation activity blockade in samples of platelet rich plasma was measured by aggregometry in 26 healthy volunteers after administration of four inductors of thrombocyte aggregation (arachidon acid, adenosindiphosphate, collagen, and ristocetin). The samples were taken before administration and 120, 240, and 360 minutes after single peroral administration of 100 or 400 mg of acetylsalicylic acid. Samples of plasma were analysed immediately after sampling. Before drug administration there was no aggregation activity in 27.7% of the sample after arachidon acid administration, 28.3% after ADP administration, 21.5 % after collagen administration and 25.3 % after ristocetin administration. After administration of 400 mg of acetylsalicylic acid and administration of arachidon acid as an inductor 89.9% of the aggregation activity of the sample was blocked after 120 minutes, 89.6 % after 240 minutes, and 90.6% after 360 minutes. After administration of adenosindiphosphate as an inductor 71.7 % of the aggregation activity of the sample was blocked after 120 minutes, 68.3% after 240 minutes, and 69.9 % after 360 minutes. And, after administration of ristocetin as an inductor 64% of the aggregation activity of the sample was blocked after 120 minutes, 66.4 % after 240 minutes, and 54% after 360 minutes. Blockade of aggregation activity after collagen administration was not statistically significant. After administration of 100 mg of acetylsalicylic acid and administration of arachidon acid 83.8 % of the aggregation activity of the sample was blocked after 120 minutes, 89.2% after 240 minutes, and 89.6 % after 360 minutes. After adenosindiphosphate administration statistically significant blockade of aggregation activity was achieved after 360 minutes in the 56.7% of the sample. Also after collagen administration 42.5 % of aggregation activity of the sample was blocked significantly after 360 minutes while ristocetin has not proved to influence aggregation in a statistically significant manner. Conclusion: Both doses of acetylsalicylic acid influenced aggregation activity of platelets in a statistically significant manner as soon as after 120 minutes following their peroral administration. However, they had different ability to influence platelets response to alternative ways of activation – by adenosindiphosphate, collagen, and ristocetin. 400 mg dose blocked these ways while 100 mg dose was efficient in blocking these ways after 360 minutes and in case of ristocetin – an inductor used to monitor platelet adhesion ability – 100 mg dose has not led to statistically significant blockade at all.

        Key words: Acetylsalicylic acid - Turbidimetric aggregometry