During intense exercise in horses the transvascular fluid flux in the pulmonary circulation (Jv-a) represents 4% of cardiac output (). This fluid flux has been attributed to an increase in pulmonary transmural hydrostatic forces, increases in perfused microvascular surface area, and reversible alterations in capillary permeability under conditions of high flow and pressure. Erythrocyte fluid efflux, however, accounts for a significant fraction of Jv-a. In the lung the Jacobs–Stewart cycle occurs with diffusion of CO2 into alveolar space with possible accompanying chloride (Cl−) and water movement from the erythrocyte directly into the pulmonary interstitium. We hypothesised that inhibition of carbonic anhydrase in erythrocytes inhibits the Jacobs–Stewart cycle and attenuates Jv-a. Five horses were exercised on a treadmill until fatigue without (control) and with acetazolamide treatment (30 mg kg−1 30 min before exercise). Erythrocyte fluid efflux, plasma fluid flux across the lung and Jv-a were calculated using haemoglobin, haematocrit, plasma protein and Q. Fluid fluxes were used to calculate erythrocyte, plasma and whole blood Cl− fluxes across the lung. Cardiac output was not different between control and acetazolamide treatment. During exercise erythrocyte fluid efflux and Jv-a increased in control (9.3 ± 3.3 and 11.0 ± 4.4 l min−1, respectively) and was higher than after acetazolamide treatment (3.8 ± 1.6 and 1.2 ± 1.2 l min−1, respectively) (P < 0.05). Plasma fluid flux did not change from rest in control and decreased after acetazolamide treatment (−4.5 ± 1.5 l min−1) (P < 0.05). Erythrocyte Cl− flux increased during exercise in control and after acetazolamide treatment (P < 0.05). During exercise plasma Cl− flux across the lung did not change in control; however, it increased with acetazolamide treatment (P= 0.0001). During exercise whole blood Cl− flux increased across the lung in control (P < 0.05) but not after acetazolamide treatment. The results indicate that Jv-a in the lung is dependent on the Jacobs–Stewart cycle and mostly independent of transmural hydrostatic forces. It also appears that Jv-a is mediated by Cl− and water egress from erythrocytes directly into the interstitium without transit through plasma.
展开▼
机译：在马匹进行剧烈运动期间，肺循环中的跨血管液通量（Jv-a）代表心输出量的4％（）。该流体通量归因于在高流量和高压条件下肺部透壁静水力的增加，灌注微血管表面积的增加以及毛细管渗透性的可逆变化。然而，红细胞外排占Jv-a的很大一部分。在肺部，Jacobs–Stewart循环发生，CO2扩散到肺泡腔，并伴有氯化物（Cl -），水从红细胞直接进入肺间质。我们假设抑制红细胞中的碳酸酐酶会抑制Jacobs–Stewart循环并减弱Jv-a。在跑步机上锻炼五匹马，直到没有疲劳（对照）和接受乙酰唑胺治疗（运动前30分钟30 mg kg -1 ）为止。使用血红蛋白，血细胞比容，血浆蛋白和Q来计算红血球流出，穿过肺和Jv-a的血浆液体通量。液体通量用于计算穿过血红蛋白，血浆和全血的Cl -通量。肺。对照和乙酰唑胺治疗之间的心输出量无差异。运动过程中，对照组的红细胞流出量和Jv-a升高（分别为9.3±3.3和11.0±4.4 l min -1 ），并高于乙酰唑胺治疗后的水平（3.8±1.6和1.2±1.2 l） min -1 ）（P <0.05）。对照组血浆血浆通量没有变化，而乙酰唑胺治疗后血浆通量下降（-4.5±1.5 l min min -1 ）（P <0.05）。对照运动期间和乙酰唑胺治疗后，红细胞Cl -通量增加（P <0.05）。在运动过程中，血浆Cl -穿过肺的通量在对照中没有变化；但是，乙酰唑胺处理后，血红蛋白增加（P = 0.0001）。在运动过程中，对照组的全血Cl -通量在肺部增加（P <0.05），但在乙酰唑胺治疗后没有增加。结果表明，肺中的Jv-a依赖于Jacobs–Stewart循环，并且主要独立于透壁静水力。似乎Jv-a是由Cl -介导的，水从红细胞直接流出到间质中，而没有穿过血浆。
展开▼
