Gashev Anatoliy A, Davis Michael J, Zawieja David C
Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M University System Health Science Center, 336 Reynolds Medical Building, College Station, TX 77843-1114, USA.
J Physiol. 2002 May 1;540(Pt 3):1023-37. doi: 10.1113/jphysiol.2001.016642.
There are only a few reports of the influence of imposed flow on an active lymph pump under conditions of controlled intraluminal pressure. Thus, the mechanisms are not clearly defined. Rat mesenteric lymphatics and thoracic ducts were isolated, cannulated and pressurized. Input and output pressures were adjusted to impose various flows. Lymphatic systolic and diastolic diameters were measured and used to determine contraction frequency and pump flow indices. Imposed flow inhibited the active lymph pump in both mesenteric lymphatics and in the thoracic duct. The active pump of the thoracic duct appeared more sensitive to flow than did the active pump of the mesenteric lymphatics. Imposed flow reduced the frequency and amplitude of the contractions and accordingly the active pump flow. Flow-induced inhibition of the active lymph pump followed two temporal patterns. The first pattern was a rapidly developing inhibition of contraction frequency. Upon imposition of flow, the contraction frequency immediately fell and then partially recovered over time during continued flow. This effect was dependent on the magnitude of imposed flow, but did not depend on the direction of flow. The effect also depended upon the rate of change in the direction of flow. The second pattern was a slowly developing reduction of the amplitude of the lymphatic contractions, which increased over time during continued flow. The inhibition of contraction amplitude was dependent on the direction of the imposed flow, but independent of the magnitude of flow. Nitric oxide was partly but not completely responsible for the influence of flow on the mesenteric lymph pump. Exposure to NO mimicked the effects of flow, and inhibition of the NO synthase by N (G)-monomethyl-L-arginine attenuated but did not completely abolish the effects of flow.
在管腔内压力受控的条件下，关于强制流动对主动淋巴泵影响的报道仅有少数几篇。因此，其机制尚未明确界定。分离大鼠肠系膜淋巴管和胸导管，插管并施加压力。调节输入和输出压力以施加不同的流量。测量淋巴管的收缩期和舒张期直径，并用于确定收缩频率和泵流量指标。强制流动抑制了肠系膜淋巴管和胸导管中的主动淋巴泵。胸导管的主动泵似乎比肠系膜淋巴管的主动泵对流量更敏感。强制流动降低了收缩的频率和幅度，相应地也降低了主动泵流量。流动诱导的对主动淋巴泵的抑制呈现两种时间模式。第一种模式是收缩频率迅速受到抑制。施加流动后，收缩频率立即下降，然后在持续流动期间随时间部分恢复。这种效应取决于强制流动的大小，但不取决于流动方向。该效应还取决于流动方向的变化率。第二种模式是淋巴管收缩幅度缓慢降低，在持续流动期间随时间增加。收缩幅度的抑制取决于强制流动的方向，但与流量大小无关。一氧化氮对流动对肠系膜淋巴泵的影响有部分但非完全的作用。暴露于一氧化氮模拟了流动的效应，而 N（G）-单甲基-L-精氨酸对一氧化氮合酶的抑制减弱但并未完全消除流动的效应。
