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心源性肺水肿与非心源性肺水肿所致肺功能障碍的比较。

Comparison of the pulmonary dysfunction caused by cardiogenic and noncardiogenic pulmonary edema.

作者信息

Bernard G R, Pou N A, Coggeshall J W, Carroll F E, Snapper J R

机构信息

Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232, USA.

出版信息

Chest. 1995 Sep;108(3):798-803. doi: 10.1378/chest.108.3.798.

Abstract

We designed a series of experiments to compare the pulmonary dysfunction observed in models of cardiogenic and noncardiogenic pulmonary edema in chronically instrumented awake sheep. Cardiogenic pulmonary edema was induced by inflating the balloon of a Foley catheter surgically positioned in the mitral valve orifice causing increased left atrial pressure (increases PLA). Noncardiogenic pulmonary edema was induced by intravenous infusion of Perilla ketone (PK). Calculated microvascular pressure remained constant during PK infusion but increased from 9.4 +/- 0.7 to 42.8 +/- 2.4 cm H2O during increases PLA. Comparable increases in lung lymph flow (QL) were observed in the two protocols (five to seven times baseline). Pulmonary edema as quantified by chest radiograph scores increased from 0 (normal) to 2.9 +/- 0.5 and 3.4 +/- 0.1 in the PK and increases PLA groups, respectively. Room air alveolar to arterial oxygen pressure difference (P[A-a]O2) increased from 24 +/- 3 to 46 +/- 7 mm Hg in the PK group and from 23 +/- 4 to 56 +/- 6 mm Hg in the increases PLA group. Dynamic compliance of the lungs (Cdyn) expressed as the percentage of the baseline value decreased to 53 +/- 7 and 50 +/- 7% in the PK and increases PLA groups, respectively. Resistance to airflow across the lungs (RL) increased from 2.5 +/- 0.6 to 3.3 +/- 0.8 cm H2O.L-1.sec-1 in the PK group and from 1.4 +/- 0.3 to 4.2 +/- 1.1 in the increases PLA group. Significant correlations were observed between changes in the severity of pulmonary edema observed on chest radiographs, Cdyn, delta P(A-a)O2, and QL in both the increases PLA groups. We conclude that similar degrees of pulmonary edema, regardless of the mechanism, are associated with similar changes in QL, Cdyn, and delta P(A-a)O2. Hydrostatic pulmonary edema appeared to cause greater changes in RL than that resulting from increased microvascular permeability.

摘要

我们设计了一系列实验,以比较在长期植入仪器的清醒绵羊的心源性和非心源性肺水肿模型中观察到的肺功能障碍。通过给手术放置在二尖瓣口的Foley导管的球囊充气,导致左心房压力升高(左心房压力升高)来诱发心源性肺水肿。通过静脉输注紫苏酮(PK)来诱发非心源性肺水肿。在输注PK期间,计算出的微血管压力保持恒定,但在左心房压力升高期间,微血管压力从9.4±0.7升高至42.8±2.4 cmH₂O。在两种方案中观察到肺淋巴流量(QL)有类似的增加(是基线的五到七倍)。通过胸部X光片评分量化的肺水肿在PK组和左心房压力升高组中分别从0(正常)增加到2.9±0.5和3.4±0.1。在PK组中,室内空气肺泡-动脉氧分压差(P[A-a]O₂)从24±3升高至46±7 mmHg,在左心房压力升高组中从23±4升高至56±6 mmHg。以基线值的百分比表示的肺动态顺应性(Cdyn)在PK组和左心房压力升高组中分别降至53±7%和50±7%。跨肺气流阻力(RL)在PK组中从2.5±0.6升高至3.3±0.8 cmH₂O·L⁻¹·s⁻¹,在左心房压力升高组中从1.4±0.3升高至4.2±1.1。在左心房压力升高组中,胸部X光片上观察到的肺水肿严重程度变化、Cdyn、ΔP(A-a)O₂和QL之间存在显著相关性。我们得出结论,无论机制如何,相似程度的肺水肿都与QL、Cdyn和ΔP(A-a)O₂的相似变化相关。静水压性肺水肿似乎比微血管通透性增加导致的肺水肿引起RL更大的变化。

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