Endothelin receptor blockade does not improve hypoxemia following acute pulmonary thromboembolism.
Endothelin receptor blockade does not improve hypoxemia following acute pulmonary thromboembolism.
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DOI：
10.1152/japplphysiol.01139.2005
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发表时间：
2007-02
影响因子：
3.3
通讯作者：
J. Tsang;W. Lamm;B. Neradilek;N. Polissar;M. Hlastala
中科院分区：
文献类型：
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作者：
J. Tsang;W. Lamm;B. Neradilek;N. Polissar;M. Hlastala
我们研究了内皮素在确定急性肺血栓栓塞症（APTE）猪模型中通气（Va）和灌注（Q）不匹配中的作用，使用非特异性内皮素拮抗剂替佐生坦。9只麻醉仔猪（约23 kg）在0 min时通过中心静脉导管接受自体血凝块（约20 g）。通过10种不同颜色的荧光微球绘制了5个不同时间点（-30，-5，30，60，120 min）的Va和Q分布。5头仔猪（第1组）在时间= 40 min时开始接受替唑生坦（由爱可泰隆提供），持续2 h，4头仔猪（第2组）仅接受生理盐水并作为对照。我们的结果表明，在所有动物中，在APTE后30分钟，但在tezosentan之前，平均Va/Q增加，因为是Va/Q异质性（log SD Va/Q），这表示其主峰的加宽。之后，tezosentan减弱了第1组的肺动脉高压，但也产生了中度全身性低血压。但是，它并没有改善动脉PO2或Va/Q不匹配。我们得出结论，内皮素拮抗作用对APTE后气体交换的影响最小，并证实了我们早期的观察结果，即APTE中低氧血症的主要机制是由于肺区域血流远离栓塞血管的机械性重新分布，导致产生许多不同的低和高Va/Q区域。
We studied the roles of endothelins in determining ventilation (Va) and perfusion (Q) mismatch in a porcine model of acute pulmonary thromboembolism (APTE), using a nonspecific endothelin antagonist, tezosentan. Nine anesthetized piglets (approximately 23 kg) received autologous clots (approximately 20 g) via a central venous catheter at time = 0 min. The distribution of Va and Q at five different time points (-30, -5, 30, 60, 120 min) was mapped by fluorescent microspheres of 10 different colors. Five piglets (group 1) received tezosentan (courtesy of Actelion) starting at time = 40 min for 2 h, and four piglets (group 2) received only saline and served as control. Our results showed that, in all of the animals at 30 min following APTE but before tezosentan, the mean Va/Q was increased, as was Va/Q heterogeneity (log SD Va/Q), which represented a widening of its main peak. Afterwards, tezosentan attenuated the pulmonary hypertension in group 1 but also produced moderate systemic hypotension. However, it did not improve arterial PO2 or Va/Q mismatch. We concluded that endothelin antagonism had minimal impact on gas exchange following APTE and confirmed our earlier observation that the main mechanism for hypoxemia in APTE was due to the mechanical redistribution of pulmonary regional blood flow away from the embolized vessels, resulting in the creation of many divergent low and high Va/Q regions.