X线造影剂影响肺阻力动脉张力的中介因子──关于内皮素和EDRF的研究

Factors Mediating Tension Changes of Pulmonary Resistant Arteries Caused by Radiographic Contrast MediaA Study on Endothelin and EDRF

目的 观察X线造影剂引起肺阻力动脉 (直径 0 .3～ 0 .6mm的微动脉 )张力改变是否由内皮素和内皮来源舒张因子 (E DRF)介导。材料与方法 肺阻力动脉从Wistar大鼠肺中分离而得 ,制备成条状浸于生理盐溶液中 ,并供给 95 %O2 /5 %CO2 混合气体。动脉条给予 17.5mmHg被动跨壁压力 ,动脉条的张力通过力传感仪自动记录。实验包括下述部分 :(1)动脉条暴露于 40mgI/mlDiatrizoate(或其甘露醇渗透压对照溶液 )中 2 0分钟 ,记录其收缩反应 ;洗去Diatrizoate(或甘露醇溶液 ) ,动脉条休息 15分钟后给予内皮素A、B受体拮抗剂SB 2 0 96 70 10 -5mol/L ,2 0分钟后动脉条再暴露于 40mgI/mlDiatrizoate(或甘露醇对照溶液 )中 2 0分钟 ,记录其收缩反应。 (2 )动脉条先由 10 -4 mol/L前列腺素F2α(PGF2α)引起收缩 ,收缩稳定后给予 80mgI/mlIoxaglate以引起血管舒张 ,记录其最大舒张值 ;洗去PGF2α及Ioxaglate ,动脉条休息 1小时后给予EDRF阻断剂L NAME 10 -4 mol/L和 7.5× 10 -6mol/LPGF2α引起实验组动脉条收缩 (收缩程度和 10 -4 mol/LPGF2α引起者相似 ) ,收缩稳定后再给予 80mgI/mlIoxaglate ,记录其最大舒张值 ,对照组用 10 -4 mol/LPGF2α引起第二次血管收缩 ,其余同实验组。结果 (1)动脉条暴露于

Objective To shed light on the question that if the tension changes of pulmonary resistant arteries (PRA, small arteries with the diameter of 0.3～0.6mm) caused by radiographic contrast media are mediated by endothelin and EDRF.Materials and Methods PRAs were dissected off from Wistar rat lungs, mounted as ring preparations and bathed in normal saline, which was gassed with the mixture of 95% O 2 and 5% CO 2. A passive transmural pressure of 17.5mmHg was given, the tensions of the rings were recorded automatically through a force transducer. The following experiments were carried out: (1) PRAs were exposed to 40mgI/ml Diatrizoate (or its mannitol osmolar control solution) for 20min, the vasoconstriction was recorded. After washing the testing solution off with normal saline, 10 -5 mol/L SB209670 was added, then 40mgI/ml Diatrizoate (or its mannitol control) was added again, after 20min the vasoconstriction was recorded. (2) PRAs were preconstricted with 10 -4 mol/L prostaglandin F 2α , 80mgI/ml Ioxaglate was added and the vasorelaxation was recorded, after washing off the testing solution, 10 -4 mol/L LNAME and 7.5×10 -6 mol/L prostaglandin F 2α , were used to create experimental group PRA preconstricition (comparable to those caused by 10 -4 mol/L prostaglandin F 2α ), 80mgI/ml Ioxaglate was added and the vasorelaxation was recorded. For the control group, the second preconstriction was induced by 10 -4 mol/L prostaglandin F 2α .Results (1) Exposure of PRA to 40mgI/ml Diatrizoate and its mannitol control for 20min caused 41.9%± 2.3% and 26.9%± 2.6% KEmax (maximum constriction caused by potassium ion), respectively. After PRA pretreated with SB209670, 42.1%± 2.7% and 27.5%± 2.9% KEmax constriction were produced, respectively. In both diatrizoate and mannitol solution groups no significant difference was found between the consecutive vasoconstriction before and after the treatment of SB209670. (2) In control group, the first and second testing 80mgI/ml Ioxaglate caused 33.4%± 4.2% and 36.7%± 3.9% relaxation, respectively (expressed in percentage of preconstriction), no significant difference was found. In experimental group the first and second testing 80mgI/ml Ioxaglate caused 38.2%± 1.6% and 43.6%± 2.2% relaxation, respectively, no significant difference was found.Conclusion This study indicates that endothelin is not the dominant factor mediating isolated PRA constriction induced by Diatrizoate or high osmolar solution, EDRF is not the dominant factor mediating ioxaglateinduced isolated PRA vasorelaxation.