Regulation of the vasomotor activity of lymph microvessels by nitric oxide and prostaglandins
Regulation of the vasomotor activity of lymph microvessels by nitric oxide and prostaglandins
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DOI：
10.1152/ajpregu.1998.274.3.r790
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发表时间：
1998-03-01
影响因子：
2.8
通讯作者：
Kaley, G
中科院分区：
文献类型：
--
作者：
Mizuno, R;Koller, A;Kaley, G
先前已经表明，内皮的存在调节小淋巴管的自发性血管舒缩。在本研究中，我们的目的是阐明内皮源性因子的性质，产生在基础条件下，并在响应激动剂，影响平滑肌张力的淋巴微血管在体外。从大鼠髂淋巴结分离传入淋巴微血管，用玻璃微量移液管插管，加压（6 cmH（2）O），并通过视频显微镜观察其直径的变化。在静息状态下，离体淋巴管表现出自发性收缩和扩张。最大和最小直径（D（max）和D（min））分别为149.8 +/- 2.9和85.8 +/- 3.6 μ m。乙酰胆碱（ACh，10（-7）至10（-5）M）和硝普钠（SNP，10（-8）至10（-6）M）暂时消除直径振荡，增加直径的药物剂量依赖性。例如，10（-5）M ACh和10（-6）M SNP分别使直径（D（max））增加15.2 ± 2.2和25.0 ± 2.7 μ m。用N（G）-硝基-L-精氨酸（10（-4）M）处理血管可显著降低直径波动的幅度，几乎完全消除乙酰胆碱诱导的淋巴微血管扩张，而SNP（10（-6）M）引起显著更大的扩张（55.6 ± 7.5 μ m）。花生四烯酸（AA，10（-8）至10（-6）M）收缩淋巴管（达50 μ m），而前列腺素E（2）（PGE（2），10（-9）至10（-7）M）扩张淋巴管（达40 μ m）。吲哚美辛（10（-5）M）增加D（max）和D（min），完全抑制AA引起的淋巴微血管收缩，但不影响PGE（2）引起的淋巴微血管扩张。用选择性PGH（2）-血栓烷A（2）（PGH（2）-TxA（2），10（-6）M）受体拮抗剂SQ-29，548处理后，AA诱导的血管收缩转变为血管扩张，而PGE（2）诱导的血管扩张则不受影响。我们的结论是，内皮型一氧化氮和洋地黄素是重要的调节剂的淋巴管运动，因此在体内的淋巴微血管泵的活动。
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 cmH(2)O), 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 (D(max) and D(min)) were 149.8 +/- 2.9 and 85.8 +/- 3.6 mu m, 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 (D(max)) by 15.2 +/- 2.2 and 25.0 +/- 2.7 mu m, respectively. Treatment of vessels with N(G)-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 mu m). Arachidonic acid (AA, 10(-8) to 10(-6) M) constricted (up to 50 mu m), whereas prostaglandin E(2) (PGE(2), 10(-9) to 10(-7) M) dilated (up to 40 mu m), lymphatic vessels. Indomethacin (10(-5) M) increased both D(max) and D(min), and completely inhibited AA-induced constrictions, but did not affect PGE(2)-induced dilations of lymph microvessels. AA-induced constrictions of lymphatics were converted into dilations after treatment with SQ-29,548, a selective PGH(2)-thromboxane A(2) (PGH(2)-TxA(2), 10(-6) M) receptor antagonist, whereas PGE(2)-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.