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血栓素B2对犬心血管及肺部的影响。

Cardiovascular and pulmonary effects of thromboxane B2 in the dog.

作者信息

Friedman L S, Fitzpatrick T M, Bloom M F, Ramwell P W, Rose J C, Kot P A

出版信息

Circ Res. 1979 Jun;44(6):748-51. doi: 10.1161/01.res.44.6.748.

Abstract

The hemodynamic properties of thromboxane B2 (TxB2), a product of prostaglandin endoperoxide metabolism, have not been thoroughly described. TxB2 is a bronchoconstrictor, but its effects on the systemic circulation and circulating platelets are unknown. Its precursor, thromboxane A2(TxA2), is a potent vasoconstrictor as well as a platelet-aggregating agent. Using intact anesthetized dogs, we investigated the effects of TxB2 on pulmonary artery pressure (PAP), airway pressure (AP), systemic arterial pressure (SAP), and myocardial contractility (MC). Vascular responses were evaluated in relation to changes in platelet population and aggregability. Intravenous TxB2 (25 and 50 micrograms/kg) increased AP (mean 62% and 69%) and PAP (50% and 86%), respectively, whereas SAP and MC responses were inconsistent. Left ventricular injections (25 micrograms/kg) also increased AP (36%) and PAP responses were inconsistent. Left ventricular injections (25 micrograms/kg) also increased AP (36%) and PAP (36%). Intraventricular administration of TxB2 produced a consistent elevation of SAP (10%) with a concomitant fall in MC (11%). These vascular responses were not consistent with alterations in platelet number or aggregability. A tachyphylactic response to TxB2 developed in AP and PAP at both dose levels and with both routes of administration. Intravenous and intraventricular TxB2 (25 micrograms/kg) produced a parallel decreasing response in PAP, suggesting the possible saturation of TxB2 binding sites or the depletion of a catabolic enzyme in the lung.

摘要

血栓素B2(TxB2)是前列腺素内过氧化物代谢的产物,其血流动力学特性尚未得到充分描述。TxB2是一种支气管收缩剂,但其对体循环和循环血小板的影响尚不清楚。其前体血栓素A2(TxA2)是一种强效血管收缩剂以及血小板聚集剂。我们使用完整的麻醉犬,研究了TxB2对肺动脉压(PAP)、气道压(AP)、体动脉压(SAP)和心肌收缩力(MC)的影响。评估了与血小板数量和聚集性变化相关的血管反应。静脉注射TxB2(25和50微克/千克)分别使AP平均升高62%和69%,PAP升高50%和86%,而SAP和MC的反应不一致。左心室注射(25微克/千克)也使AP升高36%,PAP反应不一致。左心室注射(25微克/千克)也使AP升高36%,PAP升高36%。脑室内给予TxB2使SAP持续升高10%,同时MC下降11%。这些血管反应与血小板数量或聚集性的改变不一致。在两种剂量水平和两种给药途径下,AP和PAP对TxB2均出现快速耐受反应。静脉注射和脑室内注射TxB2(25微克/千克)使PAP产生平行的下降反应,提示TxB2结合位点可能饱和或肺中分解代谢酶耗竭。

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