Saldías F J, Azzam Z S, Ridge K M, Yeldandi A, Rutschman D H, Schraufnagel D, Sznajder J I
Departamento de Enfermedades Respiratorias, Universidad Católica de Chile, Santiago, Chile.
Am J Physiol Lung Cell Mol Physiol. 2001 Sep;281(3):L591-7. doi: 10.1152/ajplung.2001.281.3.L591.
Cardiogenic pulmonary edema results from increased hydrostatic pressures across the pulmonary circulation. We studied active Na(+) transport and alveolar fluid reabsorption in isolated perfused rat lungs exposed to increasing levels of left atrial pressure (LAP; 0--20 cmH(2)O) for 60 min. Active Na(+) transport and fluid reabsorption did not change when LAP was increased to 5 and 10 cmH(2)O compared with that in the control group (0 cmH(2)O; 0.50 +/- 0.02 ml/h). However, alveolar fluid reabsorption decreased by approximately 50% in rat lungs in which the LAP was raised to 15 cmH(2)O (0.25 +/- 0.03 ml/h). The passive movement of small solutes ((22)Na(+) and [(3)H]mannitol) and large solutes (FITC-albumin) increased progressively in rats exposed to higher LAP. There was no significant edema in lungs with a LAP of 15 cmH(2)O when all active Na(+) transport was inhibited by hypothermia or amiloride (10(-4) M) and ouabain (5 x 10(-4) M). However, when LAP was increased to 20 cmH(2)O, there was a significant influx of fluid (-0.69 +/- 0.10 ml/h), precluding the ability to assess the rate of fluid reabsorption. In additional studies, LAP was decreased from 15 to 0 cmH(2)O in the second and third hours of the experimental protocol, which resulted in normalization of lung permeability to solutes and alveolar fluid reabsorption. These data suggest that in an increased LAP model, the changes in clearance and permeability are transient, reversible, and directly related to high pulmonary circulation pressures.
心源性肺水肿是由肺循环中流体静压升高所致。我们研究了在离体灌注的大鼠肺中，当左心房压力（LAP；0 - 20 cmH₂O）升高60分钟时，主动钠（Na⁺）转运和肺泡液体重吸收的情况。与对照组（0 cmH₂O；0.50 ± 0.02 ml/h）相比，当LAP升高至5和10 cmH₂O时，主动钠（Na⁺）转运和液体重吸收没有变化。然而，在LAP升高至15 cmH₂O的大鼠肺中，肺泡液体重吸收下降了约50%（0.25 ± 0.03 ml/h）。在暴露于较高LAP的大鼠中，小溶质（²²Na⁺和³H-甘露醇）和大溶质（异硫氰酸荧光素标记的白蛋白）的被动转运逐渐增加。当通过低温或amiloride（10⁻⁴ M）和哇巴因（5 × 10⁻⁴ M）抑制所有主动钠（Na⁺）转运时，LAP为15 cmH₂O的肺中没有明显水肿。然而，当LAP升高至20 cmH₂O时，有明显的液体流入（-0.69 ± 0.10 ml/h），从而无法评估液体重吸收的速率。在另外的研究中，在实验方案的第二和第三小时，LAP从15 cmH₂O降至0 cmH₂O，这导致肺对溶质的通透性和肺泡液体重吸收恢复正常。这些数据表明，在LAP升高模型中，清除率和通透性的变化是短暂的、可逆的，并且与高肺循环压力直接相关。
