Gasheva Olga Yu, Zawieja David C, Gashev Anatoliy A
Department of Systems Biology and Translational Medicine, College of Medicine, Cardiovascular Research Institute Division of Lymphatic Biology, Texas A & M Health Science Center, College Station, TX 77843-1114, USA.
J Physiol. 2006 Sep 15;575(Pt 3):821-32. doi: 10.1113/jphysiol.2006.115212. Epub 2006 Jun 29.
The objectives of this study were to evaluate the physiological importance of the flow and shear generated by phasic contractions of lymphatic vessels and the mechanisms responsible for the influences of such shear on lymphatic pumping. Lymphatic segments of the rat thoracic duct were isolated, cannulated and pressurized. The diastolic diameters were measured in phasically non-active segments. The diastolic and systolic diameters, half-relaxation time (HRT), contraction frequency, ejection fraction and fractional pump flow were determined in phasically active segments. Since imposed flow was excluded, flow and shear occurred only as a result of the intrinsic contractions in phasically active segments whereas in phasically non-active segments contraction-generated flow and shear were absent. The influences of incrementally increased transmural pressure (from 1 to 5 cmH(2)O) were examined in control conditions and after NO synthase blockade (l-NAME 10(-4) m) or cyclooxygenase blockade (indomethacin 10(-5) m). The spontaneous phasic contractions produced a flow-dependent diastolic relaxation. This reduction of the lymphatic tone is a regulatory mechanism that maintains pumping in thoracic duct in an energy-saving/efficient mode: it improves diastolic filling (enhanced lusitropy - lowering HRT), makes lymphatic contractions stronger (enhanced inotropy - higher contraction amplitude) and propels more fluid forward during each contraction (elevated ejection fraction) while decreasing contraction frequency (reduced chronotropy). The findings also demonstrated that the NO pathway, not the cyclooxygenase pathway is responsible for this reduction of lymphatic tone and is the prevailing pathway responsible for the self-regulatory adjustment of thoracic duct pumping to changes in lymph flow pattern.
本研究的目的是评估淋巴管阶段性收缩所产生的流量和剪切力的生理重要性，以及这种剪切力对淋巴泵血影响的作用机制。分离大鼠胸导管的淋巴节段，插管并加压。测量阶段性非活动节段的舒张直径。测定阶段性活动节段的舒张和收缩直径、半松弛时间（HRT）、收缩频率、射血分数和分数泵流量。由于排除了外加流量，流量和剪切力仅在阶段性活动节段的内在收缩时出现，而在阶段性非活动节段则不存在收缩产生的流量和剪切力。在对照条件下以及一氧化氮合酶阻断（L-NAME 10(-4) m）或环氧化酶阻断（吲哚美辛10(-5) m）后，检查逐渐增加的跨壁压力（从1至5 cmH(2)O）的影响。自发性阶段性收缩产生了流量依赖性舒张期松弛。这种淋巴管张力的降低是一种调节机制，可使胸导管以节能/高效模式维持泵血：它改善舒张期充盈（增强舒张性 - 降低HRT），使淋巴管收缩更强（增强收缩性 - 更高的收缩幅度），并在每次收缩时向前推动更多液体（提高射血分数），同时降低收缩频率（降低变时性）。研究结果还表明，一氧化氮途径而非环氧化酶途径负责这种淋巴管张力的降低，并且是胸导管泵血自我调节以适应淋巴流动模式变化的主要途径。
