Negrini D, Ballard S T, Benoit J N
Istituto di Fisiologia Umana, Università degli Studi, Milan, Italy.
J Appl Physiol (1985). 1994 Jun;76(6):2267-74. doi: 10.1152/jappl.1994.76.6.2267.
In 11 anesthetized spontaneously breathing rabbits, we studied the contribution to total pleural lymph flow of myogenic activity of pleural lymphatics ("intrinsic mechanism") and the effect due to mechanical action of respiratory movements ("extrinsic mechanism"). Isoncotic saline solution (5 ml) containing 100 microCi of 125I-lactate dehydrogenase (LDH) was injected into right pleural space; in all but three control rabbits, injectate contained 1 mM amiloride in dimethyl sulfoxide to induce relaxation of smooth muscle tone. At 3 h, rabbits were killed and pleural fluid was collected and its volume measured. LDH radioactivity in pleural liquid and parietal pleural tissue was counted. In control rabbits, net pleural liquid flow (Jnet) at 3 h was -0.17 +/- 0.04 (SD) ml.kg-1.h-1; LDH concentration (C) and quantity (Q) decreased by 40.3 and 51.1% of initial value, respectively; total pleural lymphatic flow (Jl), calculated from LDH clearance, was 0.58 +/- 0.01 ml.kg-1.h-1. In amiloride-treated rabbits, Jnet was 0.01 +/- 0.1 ml.kg-1.h-1, C decreased by 34.4% and Q by 33.1%, and Jl averaged 0.39 +/- 0.02 ml.kg-1.h-1. C in parietal pleura, rich in lymphatics, was 13-fold higher in control than in amiloride-treated animals. The significant decrease of pleural lymphatic flow observed with amiloride (-40% relative to control) resulted from impairment of intrinsic mechanism, whereas, at comparable breathing frequencies, extrinsic mechanism remained unaltered. The direct effect of topical application of 1 mM amiloride was confirmed on exposed mesenteric collecting lymphatic ducts (data from 5 rats): amiloride reduced lymph flow by 40% by decreasing stroke volume without greatly affecting contraction rate of lymphatic walls.
在11只麻醉状态下自主呼吸的家兔中,我们研究了胸膜淋巴管的肌源性活动(“内在机制”)对胸膜总淋巴液流量的贡献以及呼吸运动的机械作用(“外在机制”)所产生的影响。将含有100微居里125I - 乳酸脱氢酶(LDH)的等渗盐溶液(5毫升)注入右胸膜腔;除3只对照家兔外,注入液中在二甲基亚砜中含有1毫摩尔的阿米洛利,以诱导平滑肌张力松弛。3小时后,处死家兔,收集胸膜液并测量其体积。对胸膜液和壁层胸膜组织中的LDH放射性进行计数。在对照家兔中,3小时时的胸膜液净流量(Jnet)为-0.17±0.04(标准差)毫升·千克-1·小时-1;LDH浓度(C)和量(Q)分别下降至初始值的40.3%和51.1%;根据LDH清除率计算的胸膜总淋巴液流量(Jl)为0.58±0.01毫升·千克-1·小时-1。在阿米洛利处理的家兔中,Jnet为0.01±0.1毫升·千克-1·小时-1,C下降了34.4%,Q下降了33.1%,Jl平均为0.39±0.02毫升·千克-1·小时-1。富含淋巴管的壁层胸膜中的C在对照家兔中比在阿米洛利处理的动物中高13倍。观察到阿米洛利使胸膜淋巴液流量显著下降(相对于对照下降40%)是由于内在机制受损,而在可比的呼吸频率下,外在机制保持不变。在暴露的肠系膜集合淋巴管(来自5只大鼠的数据)上证实了局部应用1毫摩尔阿米洛利的直接作用:阿米洛利通过减少搏出量使淋巴液流量降低40%,而对淋巴管壁的收缩速率影响不大。