软组织挤压伤对大鼠胸主动脉反应性张力的影响

Effect of Soft Tissue Crush Injury on Tensions of Thoracic Aortic Rings in Rats

目的观察大鼠软组织挤压伤后胸主动脉反应性张力的变化,探讨一氧化氮(nitric oxide,NO)在血管反应性张力变化中的作用。方法成年SD大鼠30只,随机分为对照组、挤压后8 h组、挤压后16 h组。制备内皮完整和去内皮离体胸主动脉血管环,首先用离体血管张力检测技术测定内皮完整血管环对苯肾上腺素(phenylephrine,PE)、乙酰胆碱(acetylcholine,ACh)、Ca2+载体A23187和血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)的反应性张力变化,然后用一氧化氮合酶抑制剂N-硝基-L-精氨酸(N-nitro-L-arginine,L-NNA)预孵育血管环20 min,再检测血管环对PE、AngⅡ的收缩反应张力变化。同法检测去内皮血管环对PE和AngⅡ的反应性张力变化。结果 8h组、16h组内皮完整血管环对ACh、A23187累积剂量的舒张反应张力显著降低,对PE、AngⅡ累积剂量的收缩反应张力也降低。使用L-NNA可以增加收缩反应张力。与内皮完整血管环比较,去内皮血管环对PE、AngⅡ的收缩反应张力增加。结论大鼠软组织挤压伤可引起胸主动脉反应性张力改变,血管源性NO参与介导血管反应性张力变化。

Objective To observe the effect of soft tissue crush injury on the tensions of thoracic aortic rings（TARs） in rats and to investigate the potential roles of nitric oxide in the change of the tensions.Methods Thirty adult SD rats were randomly divided into control group and crush injury（8 h and 16 h after injury） groups.Two kinds of TARs（one with endothelium and the other without endothelium） in vitro were prepared.In the TARs with endothelium,the tensions induced by phenylephrine（PE）,acetylcholine（Ach）,calcium ionophore A23187 and angiotensin Ⅱ（AngⅡ） were measured by the vascular tension detective technique.Then the TARs with endothelium were preincubated with nitric oxide synthase inhibitor N-nitro-L-arginine（L-NNA） for 20 minutes,the tensions induced by PE and AngⅡ were measured again.In the TARs without endothelium,the tensions induced by PE and AngⅡ were measured by the same method.Results In the TARs with endothelium,the tension of relaxation induced by cumulative doses of Ach and A23187 decreased significantly in 8 h and 16 h groups.The tension of contraction induced by cumulative doses of PE and AngⅡ also decreased significantly（P0.05）.The tension of contraction increased after the preincubation with L-NNA.In the TARs without endothelium,the tension of contraction induced by PE and AngⅡincreased comparing to that of TARs with endothelium.Conclusion The soft tissue crush injury can influence the tensions of TARs in rats and the vascular-derived NO can mediate the effects.