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单侧微栓塞后肺水肿的部位。

Site of pulmonary edema after unilateral microembolization.

作者信息

Lee B C, van der Zee H, Malik A B

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1979 Sep;47(3):556-60. doi: 10.1152/jappl.1979.47.3.556.

Abstract

The effect of unilateral pulmonary microembolization on regional lung extravascular fluid accumulation was determined in dogs. Embolization was produced by injecting 100-micrometer-diam glass beads (0.25 g/kg) into the right pulmonary artery. After embolization of one lung, pulmonary arterial pressure (Ppa) and pulmonary vascular resistance increased (P less than 0.05) from base-line values of 11.7 +/- 1.3 to 17.9 +/- 1.3 Torr and of 3.4 +/- 0.5 to 5.5 +/- 0.5 Torr/(1/min). Blood flow to embolized lung measured with labeled microspheres decreased from 104.2 +/- 24.9 to 35.2 +/- 9.2 ml/min.g bloodless lung after embolization, whereas flow to the normal lung increased from 43.1 +/- 5.6 to 71.2 +/- 19.2 ml/min.g bloodless lung. Extravascular lung water-to-bloodless dry lung weight ratio (W/D) of 4.97 +/- 0.32 was greater (P less than 0.001) in the embolized lung than the value of 3.34 +/- 0.15 in nonembolized lung. In six dogs pretreated with 500 U/kg of heparin, a similar degree of duration of embolization and similar hemodynamic changes did not result in significant differences in W/D (3.88 +/- 0.18 in right lung vs. 3.02 +/- 0.53 in the left lung), and the right lung ratio was less (P less than 0.05) than the value in the heparinized dogs, suggesting that humoral mechanisms contribute to the genesis of pulmonary edema after regional embolization. Therefore, unilateral embolization leads to a greater increase in extravascular content in the embolized lung than in the nonembolized lung. Because Ppa was in the normal range after embolization, regional pulmonary edema may be due partly to the local release of factors that increase lung vascular permeability.

摘要

在犬类动物中测定了单侧肺微栓塞对局部肺血管外液体蓄积的影响。通过向右肺动脉注射直径100微米的玻璃珠(0.25克/千克)来造成栓塞。一侧肺栓塞后,肺动脉压(Ppa)和肺血管阻力从基线值11.7±1.3托和3.4±0.5托/(升/分钟)增加(P<0.05)至17.9±1.3托和5.5±0.5托/(升/分钟)。用标记微球测量的栓塞肺血流量在栓塞后从104.2±24.9降至35.2±9.2毫升/分钟·克无血肺,而正常肺的血流量从43.1±5.6增加至71.2±19.2毫升/分钟·克无血肺。栓塞肺的血管外肺水与无血干肺重量比(W/D)为4.97±0.32,高于未栓塞肺的3.34±0.15(P<0.001)。在6只预先给予500单位/千克肝素的犬中,相似程度和持续时间的栓塞以及相似的血流动力学变化并未导致W/D出现显著差异(右肺为3.88±0.18,左肺为3.02±0.53),且右肺的比值低于肝素化犬的数值(P<0.05),这表明体液机制促成了局部栓塞后肺水肿的发生。因此,单侧栓塞导致栓塞肺血管外含量的增加幅度大于未栓塞肺。由于栓塞后Ppa处于正常范围内,局部肺水肿可能部分归因于增加肺血管通透性的因子的局部释放。

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