Introduction. Platelet activation is the initial stage of thrombotic complications in pathological conditions, primarily in atherosclerotic cardiovascular diseases. Endogenous hydrogen sulfide (H2S) is an antiplatelet agent, but the specific ways to realize its effects are not studied enoughAim: To study the effect of H2S on adenosine diphosphate (ADP)-induced platelet aggregation in patients with coronary heart disease (CHD) with blockers of Na+,K+,2Cl- cotransporter (NKCC), an anion exchanger, and a phosphodiesterase (PDE) inhibitor of cyclic nucleotides.Material and Methods. The study included 22 patients with CHD. The control group included 14 healthy volunteers. Platelet aggregation was determined by turbidimetric method. The degree of aggregation (%) and the size of aggregates (rel. units) were measured. ADP (2 μM) was an aggregation inductor. In some cases the incubation medium contained the hydrogen sulfide donor NaHS (1–100 μM) and aggregation modifierResults. The H2S donor at a concentration of 100 μM reduced the parameters of ADP-dependent platelet aggregation in healthy volunteers and increased it in patients with coronary artery disease. NKCC and anion exchanger blockers, as well as a PDE inhibitor, reduced ADP-dependent platelet aggregation in healthy volunteers. The combined action of these agents and NaHS enhanced the inhibitory effects of the applied modifiers. The results obtained for platelet aggregation in patients with coronary artery disease differed in different directionConclusion. The obtained data indicate that the antiaggregation effect of H2S is realized through the effect on the NKCC and anion exchanger, as well as due to the effect on the links of the signaling system mediated by cyclic nucleotides.
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