Contraction-initiated NO-dependent lymphatic relaxation: a self-regulatory mechanism in rat thoracic duct
Contraction-initiated NO-dependent lymphatic relaxation: a self-regulatory mechanism in rat thoracic duct
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DOI：
10.1113/jphysiol.2006.115212
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发表时间：
2006-09-15
影响因子：
5.5
通讯作者：
Gashev, Anatoliy A.
中科院分区：
文献类型：
--
作者：
Gasheva, Olga Yu.;Zawieja, David C.;Gashev, Anatoliy A.
本研究的目的是评估的生理重要性的流动和剪切产生的相位收缩的淋巴管和负责的机制，这种剪切对淋巴泵的影响。分离大鼠胸导管的淋巴段，插管并加压。在相位非活动节段中测量舒张期直径。在相性活动节段中测定舒张期和收缩期直径、半松弛时间（HRT）、收缩频率、射血分数和泵血分数。由于施加的流量被排除在外，流动和剪切只发生作为一个结果的内在收缩阶段性活动的部分，而在阶段性非活动的部分收缩产生的流动和剪切不存在。在对照条件下以及在NO合酶阻断（L-NAME 10（-4）M）或环氧合酶阻断（吲哚美辛10（-5）M）后，检测了跨壁压递增（从1到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。淋巴张力的这种降低是以节能/高效模式维持胸导管中泵送的调节机制：其改善舒张期充盈（增强的收缩力-降低HRT），使淋巴收缩更强（增强的收缩力-更高的收缩幅度），并在每次收缩期间向前推进更多的液体（升高的射血分数），同时降低收缩频率（降低的变时性）。研究结果还表明，NO途径，而不是环氧合酶途径是负责这种淋巴张力的降低，是负责胸导管泵送的自我调节调节淋巴流动模式变化的主要途径。
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.