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Beta-lactam antibiotic-mediated changes in platelet reactivity and vascular endothelial functions.

机译:β-内酰胺类抗生素介导的血小板反应性和血管内皮功能的变化。

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摘要

To evaluate vascular and platelet compatibility of intravenous administration of beta-lactam antibiotics, we assessed the effects of therapeutic concentrations of ceftriaxone, aztreonam, and ceftazidime on platelet reactivity to different agonists (sodium arachidonate, collagen and adenosine diphosphate) and on selected vascular endothelial functions (adenosine diphosphatase activity, prostacyclin production and t-PA release). Ceftriaxone and, to a lesser degree, aztreonam, enhanced platelet reactivity, evaluated as onset of platelet aggregating response, and increased thromboxane production to subthreshold concentrations of arachidonate. There was no modification in platelet reactivity after ceftazidime treatment. Ceftriaxone and ceftazidime, but not aztreonam, inhibited endothelial adenosine diphosphatase activity. Prostacyclin production and t-PA release were inhibited only by ceftriaxone at high concentrations. While it is difficult to establish which marker (platelet or endothelial functions) has more clinical reference in human vascular compatibility, it seems feasible to consider aztreonam the most compatible of the beta-lactams studied.
机译:为了评估静脉内使用β-内酰胺类抗生素的血管和血小板的相容性,我们评估了头孢曲松,氨曲南和头孢他啶的治疗浓度对不同激动剂(花生四烯酸钠,胶原蛋白和二磷酸腺苷)的血小板反应性以及所选血管内皮功能的影响。 (腺苷二磷酸酶活性,前列环素产生和t-PA释放)。头孢曲松和氨曲南在较小程度上增强了血小板的反应性,被评估为血小板聚集反应的开始,血栓烷的产生增加到阈值以下的花生四烯酸。头孢他啶治疗后血小板反应性没有改变。头孢曲松和头孢他啶,但不是氨曲南,抑制内皮腺苷二磷酸酶活性。前列环素的产生和t-PA的释放仅在高浓度下被头孢曲松抑制。虽然很难确定哪种标记物(血小板或内皮功能)在人类血管相容性方面具有更多的临床参考价值,但认为氨曲南与所研究的β-内酰胺类药物的相容性最高似乎是可行的。

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