Frlic Olga, Seliškar Alenka, Domanjko Petrič Aleksandra, Blagus Rok, Heigenhauser George, Vengust Modest
Veterinary Faculty, University of Ljubljana, Ljubljana, Slovenia.
Institute for Biostatistics and Medical Informatics, University of Ljubljana, Ljubljana, Slovenia.
Front Physiol. 2018 Feb 21;9:124. doi: 10.3389/fphys.2018.00124. eCollection 2018.
General anesthesia (GA) can cause abnormal lung fluid redistribution. Pulmonary circulation transvascular fluid fluxes ( ) are attributed to changes in hydrostatic forces and erythrocyte volume (EV) regulation. Despite the very low hydraulic conductance of pulmonary microvasculature it is possible that GA may affect hydrostatic forces through changes in pulmonary vascular resistance (PVR), and EV through alteration of erythrocyte transmembrane ion fluxes ( ). Furosemide (Fur) was also used because of its potential to affect pulmonary hydrostatic forces and . A hypothesis was tested that , with or without furosemide treatment, will not change with time during GA. Twenty dogs that underwent castration/ovariectomy were randomly assigned to Fur ( = 10) (4 mg/kg IV) or placebo treated group (Con, = 10). Baseline arterial (BL) and mixed venous blood were sampled during GA just before treatment with Fur or placebo and then at 15, 30 and 45 min post-treatment. Cardiac output (Q) and pulmonary artery pressure (P) were measured. and were calculated from changes in plasma protein, hemoglobin, hematocrit, plasma and whole blood ions, and Q. Variables were analyzed using random intercept mixed model ( < 0.05). Data are expressed as means ± SE. Furosemide caused a significant volume depletion as evident from changes in plasma protein and hematocrit ( < 0.001). However; Q, P, and were not affected by time or Fur, whereas erythrocyte fluid flux was affected by Fur ( = 0.03). Furosemide also affected erythrocyte transmembrane K and Cl, and transvascular Cl metabolism ( ≤ 0.05). No other erythrocyte transmembrane or transvascular ion fluxes were affected by time of GA or Fur. Our hypothesis was verified as was not affected by GA or ion metabolism changes due to Fur treatment. Furosemide and 45 min of GA did not cause significant hydrostatic changes based on Q and P. Inhibition of Na/K/2Cl cotransport caused by Fur treatment, which can alter EV regulation and , was offset by the Jacobs Stewart cycle. The results of this study indicate that the Jacobs Stewart cycle/erythrocyte Cl metabolism can also act as a safety factor for the stability of lung fluid redistribution preserving optimal diffusion distance across the blood gas barrier.
全身麻醉（GA）可导致肺内液体异常重新分布。肺循环跨血管液体通量（ ）归因于流体静力压的变化和红细胞体积（EV）调节。尽管肺微血管的水力传导率极低，但GA仍有可能通过改变肺血管阻力（PVR）来影响流体静力压，并通过改变红细胞跨膜离子通量（ ）来影响EV。还使用了呋塞米（Fur），因为它有可能影响肺流体静力压和 。我们检验了一个假设，即在GA期间，无论是否使用呋塞米治疗， 都不会随时间变化。将20只接受去势/卵巢切除术的犬随机分为Fur组（ = 10）（静脉注射4 mg/kg）或安慰剂治疗组（Con， = 10）。在GA期间，在给予Fur或安慰剂治疗前以及治疗后15、30和45分钟采集基线动脉血（BL）和混合静脉血。测量心输出量（Q）和肺动脉压（P）。根据血浆蛋白、血红蛋白、血细胞比容、血浆和全血离子以及Q的变化计算 和 。使用随机截距混合模型分析变量（ < 0.05）。数据以均值±标准误表示。从血浆蛋白和血细胞比容的变化可以明显看出，呋塞米导致了显著的容量消耗（ < 0.001）。然而，Q、P和 不受时间或Fur的影响，而红细胞液体通量受Fur影响（ = 0.03）。呋塞米还影响红细胞跨膜K和Cl以及跨血管Cl代谢（ ≤ 0.05）。GA时间或Fur均未影响其他红细胞跨膜或跨血管离子通量。我们的假设得到了验证，因为 不受GA或呋塞米治疗引起的离子代谢变化的影响。基于Q和P，呋塞米和45分钟的GA并未引起显著的流体静力压变化。呋塞米治疗引起的Na/K/2Cl共转运抑制可改变EV调节和 ，但被雅各布斯 - 斯图尔特循环抵消。本研究结果表明，雅各布斯 - 斯图尔特循环/红细胞Cl代谢也可作为肺液体重新分布稳定性的安全因素，维持血气屏障的最佳扩散距离。
