Mizuno R, Koller A, Kaley G
Department of Physiology, New York Medical College, Valhalla 10595, USA.
Am J Physiol. 1998 Mar;274(3):R790-6. doi: 10.1152/ajpregu.1998.274.3.R790.
It was shown previously that the presence of endothelium modulates spontaneous vasomotion of small lymphatic vessels. In the present study, we aimed to elucidate the nature of endothelium-derived factors, produced in basal conditions and in response to agonists, that affect the smooth muscle tone of lymph microvessels in vitro. Afferent lymph microvessels were isolated from rat iliac lymph nodes, cannulated with glass micropipettes, and pressurized (6 cmH2O), and changes in their diameter were investigated with video microscopy. In resting conditions, isolated lymph vessels exhibited spontaneous constrictions and dilations. The maximum and minimum diameters (Dmax and Dmin) were 149.8 +/- 2.9 and 85.8 +/- 3.6 microns, respectively. Acetylcholine (ACh, 10(-7) to 10(-5) M) and sodium nitroprusside (SNP, 10(-8) to 10(-6) M) temporarily abolished diameter oscillations, increasing the diameter of lymphatics dose dependently. For example, 10(-5) M ACh and 10(-6) M SNP increased the diameter (Dmax) by 15.2 +/- 2.2 and 25.0 +/- 2.7 microns, respectively. Treatment of vessels with NG-nitro-L-arginine (10(-4) M) significantly reduced the amplitude of diameter oscillations and nearly completely eliminated ACh-induced dilation of lymph microvessels, whereas SNP (10(-6) M) elicited a significantly greater dilation (55.6 +/- 7.5 microns). Arachidonic acid (AA, 10(-8) to 10(-6) M) constricted (up to 50 microns), whereas prostaglandin E2 (PGE2, 10(-9) to 10(-7) M) dilated (up to 40 microns), lymphatic vessels. Indomethacin (10(-5) M) increased both Dmax and Dmin and completely inhibited AA-induced constrictions, but did not affect PGE2-induced dilations of lymph microvessels. AA-induced constrictions of lymphatics were converted into dilations after treatment with SQ-29,548, a selective PGH2-thromboxane A2 (PGH2-TxA2, 10(-6) M) receptor antagonist, whereas PGE2-induced dilations were not affected. We conclude that endothelial nitric oxide and prostaglandins are important modulators of lymphatic vasomotion, hence pumping activity of lymph microvessels in vivo.
先前的研究表明，内皮的存在可调节小淋巴管的自发性血管运动。在本研究中，我们旨在阐明在基础条件下以及对激动剂作出反应时产生的内皮衍生因子的性质，这些因子在体外影响淋巴微血管的平滑肌张力。从大鼠髂淋巴结分离出传入淋巴微血管，用玻璃微量移液器插管并加压（6 cmH₂O），并用视频显微镜观察其直径变化。在静息状态下，分离的淋巴管表现出自发性收缩和舒张。最大和最小直径（Dmax和Dmin）分别为149.8±2.9微米和85.8±3.6微米。乙酰胆碱（ACh，10⁻⁷至10⁻⁵ M）和硝普钠（SNP，10⁻⁸至10⁻⁶ M）可暂时消除直径振荡，使淋巴管直径呈剂量依赖性增加。例如，10⁻⁵ M ACh和10⁻⁶ M SNP分别使直径（Dmax）增加15.2±2.2微米和25.0±2.7微米。用NG-硝基-L-精氨酸（10⁻⁴ M）处理血管可显著降低直径振荡幅度，并几乎完全消除ACh诱导的淋巴微血管舒张，而SNP（10⁻⁶ M）引起的舒张明显更大（55.6±7.5微米）。花生四烯酸（AA，10⁻⁸至10⁻⁶ M）使淋巴管收缩（可达50微米），而前列腺素E2（PGE2，10⁻⁹至10⁻⁷ M）使淋巴管舒张（可达40微米）。吲哚美辛（10⁻⁵ M）增加了Dmax和Dmin，并完全抑制了AA诱导的收缩，但不影响PGE2诱导的淋巴微血管舒张。用选择性PGH2-血栓素A2（PGH2-TxA2，10⁻⁶ M）受体拮抗剂SQ-29,548处理后，AA诱导的淋巴管收缩转变为舒张，而PGE2诱导的舒张不受影响。我们得出结论，内皮一氧化氮和前列腺素是淋巴血管运动的重要调节因子，因此也是体内淋巴微血管泵血活动的重要调节因子。
