<原著>陳旧性心筋梗塞におけるtaurineの抗血小板作用機序
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The inhibitory effects of taurine on platelet aggregation were compared between patients with old myocardial infarction (OMI) and normals (N). Platelet aggregation was measured by Born's method, platelet malondialdehyde formation with arachidonic acid by the TBA method and mean platelet volume and platelet count were by a Coulter counter. Plasma taurine, cystine and the other essential amino acid contents and platelet taurine content were measured by the amino acid analyzer. In vitro, platelet aggregation was induced by ADP and A23187,and platelet malondialdehyde formation induced by 125 μM arachidonic acid was measured under the incubation with and without 10 mM taurine. In order to estimate the change of cytoplasmic Ca^<2+> in thrombin activated platelet, the intensity of quin 2 fluorescence was measured by Rink's method. OMI showed the following significant differences from N. Platelet aggregations induced by 2.3 μM ADP and 5.0 μM A23187 were increased (p<0.05 and P<0.001), platelet malondialdehyde formation and mean platelet volume increased (P<0.001 and p<0.05), platelet count decreased (P<0.01), plasma taurine content decreased (p<0.01) and plasma cystine content increased (p<0.01). There were no significant differences in all plasma essential amino acid contents and platelet taurine content between the two groups. In vitro, platelet aggregations induced by 4.6 μM ADP, 2.5 μM A23187 and 5.0 μM A23187 were significantly inhibited (P<0.01,P<0.05 and P<0.05) with 10 mM taurine, and also the increase of cytoplasmic Ca^<2+> in the platelet activated with thrombin was inhibited in OMI. Platelet malondialdehyde formation was not significantly affected by the incubation with 10 mM taurine in both groups. These results suggest that the predominance of relatively large brisk platelets may result from the platelet production induced by the chronic consumption of platelets in OMI. The difference of platelet response to taurine between the two groups could be attributed to the derangement of platelet kinetics or metabolism in OMI. It seems reasonable to conclude from those abovementioned that the inhibitory mechanism of taurine from platelet aggregation in OMI is not the effect on arachidonic acid metabolism, but the suppression of cytoplasmic Ca^<2+> change in activated platelet.
- 近畿大学の論文
- 1987-09-25
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