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本文旨在离体观察失血性休克后不同时间淋巴管的收缩性变化及一氧化氮(nitric oxide,NO)的作用。分离失血性休克进程中不同时间点(0,0.5,1,2,3h)的大鼠胸导管条,采用微血管压力-直径测定技术,离体观察淋巴管在不同跨壁压(1,3,5,7,9cmH2O)下的收缩频率(contraction frequency,CF)、收缩末期口径(end diastolic diameter,EDD)、舒张末期口径(end systolicdiameter,ESD)、被动管径(passive diameter,PD)的变化,计算淋巴管的收缩幅度(contraction amplitude,CA)、紧张性指数(tonicindex,TI)和泵流分数(fractional pump flow,FPF)。结果显示,在多个跨壁压下,休克0h、休克0.5h淋巴管的CF、TI、FPF显著高于对照组,随着休克的发展,休克2h和休克3h淋巴管在多个跨壁压下的CF、TI、FPF显著低于对照组。用NO相关的工具药单独或联合孵育休克0.5h和休克2h的淋巴管,然后在3cmH2O跨壁压条件下测定淋巴管的收缩性。NO供体L-Arg使休克0.5h淋巴管的CF、TI、FPF逆转至对照组水平,可溶性鸟苷酸环化酶抑制剂ODQ可抑制L-Arg的作用;相反地,NOS抑制剂L-NAME可提高休克2h淋巴管的CF、TI、FPF,磷酸二酯酶抑制剂氨茶碱则抑制L-NAME的作用。以上结果表明,失血性休克过程中淋巴管的收缩性呈双相变化,即早期收缩性增高,后期为低收缩性;NO在休克淋巴管收缩性双相变化中具有显著的调节作用。
The purpose of this study was to observe in vitro the contractile changes of lymphatic vessels and the role of nitric oxide (NO) at different times after hemorrhagic shock. The thoracic duct strips of rats at different time points (0, 0.5, 1, 2, 3 h) during hemorrhagic shock were isolated and the lymphatic vessels were observed at different transmural pressures (1, 3, (CF), end diastolic diameter (EDD), end systolic diameter (ESD), and passive diameter (PD) under 5, 7 and 9 cmH2O, The contraction amplitude (CA), tonic index (TI) and fractional pump flow (FPF) of lymphatic vessels were calculated. The results showed that the CF, TI and FPF of lymphatic vessels at 0h and 0.5h after shock were significantly higher than those of control group at several transmural pressures. With the development of shock, Under the CF, TI, FPF significantly lower than the control group. Lymph tubes were incubated with NO-related tools alone or in combination for 0.5 h at shock and 2 h at shock, and lymphatic vessel contractility was measured at 3 cm H20 transmural pressure. NO donor L-Arg reversed the level of CF, TI and FPF in the lymphatic vessels 0.5h after the shock to the level of the control group. Soluble guanylate cyclase inhibitor ODQ inhibited the effect of L-Arg; on the contrary, the NOS inhibitor L- NAME could increase the CF, TI, FPF of lymphatic vessels at 2h after shock, and aminophylline, a phosphodiesterase inhibitor, inhibited the effect of L-NAME. The above results show that the contraction of lymphatic vessels during hemorrhagic shock showed a biphasic change, that is, early contractility increased in the late stage of low-shrinkage; NO in shock lymphatic contraction biphasic changes have a significant regulatory role.