Kikuchi Y, Traber L D, Herndon D N, Traber D L
Department of Anesthesiology, University of Texas Medical Branch, Galveston, USA.
Am J Physiol. 1996 Dec;271(6 Pt 2):R1620-4. doi: 10.1152/ajpregu.1996.271.6.R1620.
We previously reported that smoke inhalation to the right lung will result in damage to the air-insufflated left lung. In this study we confirm these findings and determine whether this injury is associated with an elevation in lung lymph flow and pulmonary microvascular permeability to protein as indexed by changes in reflection coefficient. Sheep (n = 12) were surgically prepared by placement of a Swan-Ganz catheter and pneumatic occluders on all pulmonary veins and the left pulmonary artery. The left lung lymphatic was selectively cannulated as shown previously (Y. Kikuchi, H. Nakazawa, and D. Traber. Am. J. Physiol. 269 (Regulatory Integrative Comp. Physiol. 38): R943-R947, 1995). All afferent lymphatics from the right lung were severed, and the right pulmonary ligament was sectioned. The caudal end of the lymph node was sectioned to remove systemic lymph contamination. The sheep were studied in the unanesthetized state 7 days later. To ensure that lymph flow was exclusively from the left lung (QLL), right pulmonary microvascular pressure was increased, a procedure that resulted in little or no change in QLL, as was previously shown. The sheep were then anesthetized, and a Carlens tube was positioned to allow separate ventilation of the right and left lung. The right lungs of five sheep and the left lungs of two sheep were insufflated with cotton smoke. Insufflation of the left lung with cotton smoke produced a fourfold increase in QLL that began 4 h after insult. Insufflation of the right lung with smoke led to a doubling of QLL that began 12 h after insult. Changes in QLL were associated with increased microvascular permeability, as indexed by the reflection coefficient. Control sheep (air insufflated into both lungs, n = 5) showed no change in QLL. Injury to the right lung resulted in damage to the left air-insufflated lung, suggesting a hematogenous mediation of the response.
我们之前报道过，向右侧肺吸入烟雾会导致充入空气的左侧肺受损。在本研究中，我们证实了这些发现，并确定这种损伤是否与肺淋巴液流量增加以及肺微血管对蛋白质的通透性增加（以反射系数的变化为指标）有关。通过在所有肺静脉和左肺动脉上放置Swan - Ganz导管和气动闭塞器，对12只绵羊进行手术准备。如之前所示（菊池洋、中泽浩、特拉伯·D.《美国生理学杂志》269卷（调节整合与比较生理学38期）：R943 - R947，1995年），选择性地插入左肺淋巴管。切断来自右肺的所有传入淋巴管，并切开右肺韧带。切开淋巴结的尾端以去除全身淋巴污染。7天后在未麻醉状态下对绵羊进行研究。为确保淋巴液流量仅来自左肺（QLL），增加右肺微血管压力，该操作如之前所示导致QLL几乎没有变化。然后对绵羊进行麻醉，并放置卡伦斯管以允许分别对右肺和左肺进行通气。对5只绵羊的右肺和2只绵羊的左肺充入棉烟。对左肺充入棉烟后，QLL在损伤后4小时开始增加四倍。对右肺充入烟雾导致QLL在损伤后12小时开始增加一倍。QLL的变化与微血管通透性增加有关，以反射系数为指标。对照绵羊（双侧肺均充入空气，n = 5）的QLL无变化。右肺损伤导致充入空气的左肺受损，提示该反应存在血源性介导。
