Ketanserin prevents platelet aggregation and endotoxin‐induced pulmonary vasoconstriction
Ketanserin prevents platelet aggregation and endotoxin‐induced pulmonary vasoconstriction
复制标题
酮色林可防止血小板聚集和内毒素引起的肺血管收缩
DOI：
10.1097/00003246-198308000-00005
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发表时间：
1983
影响因子：
8.8
通讯作者：
Mohammad Sf
中科院分区：
文献类型：
--
作者：
T. Meuleman;Hill Dc;Port Jd;Theodore H. Stanley;Nathan L. Pace;Mohammad Sf
继发于脓毒症的肺动脉高压部分是由于血小板释放5-羟色胺。本研究探讨了酮色林，一种新的，高度特异性的5-羟色胺拮抗剂，对血小板聚集和心血管疾病的影响与细菌内毒素血症在狗。酮色林显著抑制5-羟色胺和肾上腺素混合诱导的体外血小板聚集。当在内毒素输注之前将酮色林给予动物时，心输出量更大，平均肺动脉压（MPAP）、肺和全身血管阻力（PVR和SVR）和动静脉氧含量差[C（α-&OV0456;）O2]小于未接受酮色林的动物。当在内毒素输注后给予酮色林时，获得了PVR、SVR和C（α-&OV0456;）O2的类似结果。这些数据表明，酮色林抑制阿托卡宁诱导的血小板聚集，并修改许多与细菌内毒素血症相关的心血管变化。
Pulmonary hypertension secondary to sepsis is due, in part, to release of serotonin from platelets. This study examines the effects of ketanserin, a new, highly specific serotonin antagonist, on platelet aggregation and the cardiovascular changes associated with bacterial endotoxemia in dogs. Ketanserin markedly inhibits in vitro platelet aggregation induced by mixing serotonin and epinephrine. When ketanserin is administered to animals before endotoxin infusion, cardiac output is greater and mean pulmonary artery pressure (MPAP), pulmonary and systemic vascular resistance (PVR and SVR) and arteriovenous oxygen content difference [C(a-&OV0456;)O2] are less than in animals not receiving ketanserin. Similar results for PVR, SVR, and C(a-&OV0456;)O2 are obtained when ketanserin is administered after endotoxin infusion. The data indicate that ketanserin inhibits serotonin-induced platelet aggregation and modifies many cardiovascular changes associated with bacterial endotoxemia.