Ikeda M, Umegaki K, Takeshita N, Mitsubori M, Tomita T, Tomita I
University of Shizuoka School of Pharmaceutical Sciences, Japan.
Thromb Res. 1989 Nov 1;56(3):441-52. doi: 10.1016/0049-3848(89)90257-0.
Platelet aggregation in whole blood, platelet rich plasma, and gel-filtered platelets were markedly attenuated in SHRSP compared with those in age-matched normotensive WKY. The result was consistent with the previous report of washed platelets. Despite prevention of high blood pressure, a long duration of hypotensive treatment only slightly improved aggregability of washed platelets but did not restore it to the range of age-matched WKY platelets. Blood pressure, heart ratios and thrombin-induced washed platelet aggregation were examined in SHRSP, WKY, and the cross (F1: WKY x SHRSP). The higher blood pressure and heart ratios the lower platelet aggregability was observed in the three strains, and there was no overlapping distribution of these values. F1 progeny exhibited intermediate values in blood pressure, heart ratio and platelet aggregability between the parental values. These results suggested that hypofunctions of SHRSP platelet were not secondary changes due to high blood pressure, but primary changes which are genetically linked to high blood pressure.
与年龄匹配的血压正常的WKY相比，SHRSP全血、富血小板血浆和凝胶过滤血小板中的血小板聚集明显减弱。该结果与之前关于洗涤血小板的报道一致。尽管预防了高血压，但长时间的降压治疗仅略微改善了洗涤血小板的聚集性，并未将其恢复到年龄匹配的WKY血小板的范围。在SHRSP、WKY及其杂交后代（F1：WKY×SHRSP）中检测了血压、心率和凝血酶诱导的洗涤血小板聚集。在这三个品系中，血压和心率越高，血小板聚集性越低，且这些值没有重叠分布。F1后代在血压、心率和血小板聚集性方面表现出介于亲本值之间的中间值。这些结果表明，SHRSP血小板的功能减退不是高血压引起的继发性变化，而是与高血压基因相关的原发性变化。
