Hao Ning, Deng Chun-Yu, Kuang Su-Juan, Ma Jue, Zhang Guang-Yan, Cui Jian-Xiu
Postgraduate Institute, Southern Medical University, Guangzhou 510515, China.E-mail:
Nan Fang Yi Ke Da Xue Xue Bao. 2017 Mar 20;37(3):342-346. doi: 10.3969/j.issn.1673-4254.2017.03.11.
To investigate the effects of propofol combined with indomethacin on the contractile function of isolated human pulmonary arteries.
Human pulmonary artery preparations were obtained from patients undergoing surgery for lung carcinoma. The intrapulmonary arteries were dissected and cut into rings under microscope for treatment with propofol or propofol combined with indomethacin. In each group, the rings were divided into endothelium-intact and endothelium-denuded groups and mounted in a Multi Myograph system. In propofol group, the rings were preconstricted by U46619 to induce a sustained contraction, and propofol (10-300 mmol/L) was then applied cumulatively. In the combined treatment group, the rings were pretreated with indomethacin (100 µmol/L) for 30 min before application of U46619 to induce sustained contraction, and propofol (10-300 µmol/L) was added cumulatively after the tension became stable.
Propofol (10-100 µmol/L) induced constrictions at low concentrations and caused relaxations at higher concentrations (100-300 µmol/L) in the pulmonary artery rings with prior U46619-induced contraction. Propofol caused stronger constrictions in endothelium-intact rings [EC=4.525∓0.37, Emax=(30.44∓2.92)%] than in endothelium-denuded rings [EC=4.699∓0.12, Emax=(31.19∓5.10)%, P<0.05]. Pretreatment of the rings with indomethacin abolished constrictions, and the relaxation was more obvious in endothelium-intact group [pD=3.713∓0.11, Emax=(98.72∓0.34)%] than in endothelium- denuded group [pD=3.54∓0.03, Emax=(94.56∓0.53)%, P<0.05].
Propofol induces constriction at low concentrations and relaxation at high concentrations in human intrapulmonary arteries with U46619-induced contraction. Indomethacin abolishes the constriction induced by propofol in isolated intrapulmonary arteries, suggesting that propofol potentiates U46619-mediated pulmonary vasoconstriction by promoting the concomitant production of prostaglandin by cyclooxygenase in pulmonary artery smooth muscle cells, and the mechanism for its relaxation effect may partly depend on the endothelium.
研究丙泊酚联合吲哚美辛对离体人肺动脉收缩功能的影响。
从肺癌手术患者获取人肺动脉标本。在显微镜下解剖肺内动脉并切成环，分别用丙泊酚或丙泊酚联合吲哚美辛处理。每组中环又分为内皮完整组和去内皮组，并安装在多功能肌张力测定系统中。丙泊酚组，先用U46619预收缩环以诱导持续收缩，然后累积应用丙泊酚（10 - 300 μmol/L）。联合治疗组，在应用U46619诱导持续收缩前先用吲哚美辛（100 μmol/L）预处理30分钟，待张力稳定后再累积加入丙泊酚（10 - 300 μmol/L）。
在预先用U46619诱导收缩的肺动脉环中，丙泊酚（10 - 100 μmol/L）在低浓度时诱导收缩，在高浓度（100 - 300 μmol/L）时引起舒张。丙泊酚在内皮完整环中引起的收缩更强[EC = 4.525±0.37，Emax =(30.44±2.92)%]，相比去内皮环[EC = 4.699±0.12，Emax =(31.19±5.10)%，P<0.05]。用吲哚美辛预处理环可消除收缩，且内皮完整组的舒张更明显[pD = 3.713±0.11，Emax =(98.72±0.34)%]，相比去内皮组[pD = 3.54±0.03，Emax =(94.56±0.53)%，P<0.05]。
在有U46619诱导收缩的人肺内动脉中，丙泊酚在低浓度时诱导收缩，高浓度时引起舒张。吲哚美辛消除了丙泊酚在离体肺内动脉中诱导的收缩，提示丙泊酚通过促进肺动脉平滑肌细胞中环氧化酶伴随产生前列腺素而增强U46619介导的肺血管收缩，其舒张作用机制可能部分依赖于内皮。
