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目的观察七氟醚(SEV)预先给药对血管紧张素Ⅱ(AngⅡ)诱发大鼠离体主动脉收缩反应的影响。方法取雄性Wistar大鼠胸主动脉,制成4mm长的血管段,随机分为2组,正常组和去内膜组。实验分三部分进行。第一部分:两组均分为对照组和SEV组两个亚组,对照组不再进行任何处理,SEV组通入5.1%SEV,15min后给予不同浓度AngⅡ,每一血管段只随机接受一次单一剂量的AngⅡ刺激,测定血管收缩反应的峰值水平。第二部分:两组均将血管段先浸入含10-4mol/LN-硝基L-精氨酸甲酯(L-NAME)的KBS中15min,然后给予10-7mol/LAngⅡ,测定血管收缩反应的峰值。第三部分:将两组血管段先浸入通有不同浓度(0、1.7%、3.4%和5.1%)SEV的KBS中15min,然后给予10-7mol/LAngⅡ,观察SEV对AngⅡ诱发血管收缩反应的抑制效应。结果第一部分:与对照组比较,正常、去内膜组AngⅡ浓度分别在3×10-8-10-6mol/L和3×10-9-10-6mol/L时SEV组主动脉收缩反应降低(P<0.05或0.01);与正常组比较,去内膜组AngⅡ浓度在3×10-9-10-6mol/L时对照、SEV组主动脉收缩反应均升高(P<0.05或0.01)。第二部分:AngⅡ诱发的正常组血管段收缩反应由未经L-NAME处理的43%±5%增至经L-NAME处理的71%±6%(P<0.01);而去内膜组血管段收缩反应在未经和经L-NAME处理组无变化。第三部分:去内膜组在SEV浓度为0-5.1%时主动脉收缩反应均高于正常组(P<0.05);与SEV浓度为0时比较,正常组在SEV浓度为3.4%和5.1%时主动脉脉收缩反应降低,去内膜组在SEV浓度为1.7%-5.1%时主动脉收缩反应降低(P<0.05或0.01)。结论SEV能够抑制AngⅡ诱发的剂量依赖性大鼠离体主动脉收缩反应,去除血管内膜抑制作用加重;SEV还抑制AngⅡ刺激内膜释放NO所产生的血管舒张作用。
Objective To observe the effect of sevoflurane (SEV) preconditioning on angiotensin Ⅱ (Ang Ⅱ) -induced aortic contractile response in isolated rat aorta. Methods Thoracic aorta of male Wistar rats were made into 4mm long vascular segments and randomly divided into 2 groups, normal group and endometrium group. The experiment is divided into three parts. The first part: The two groups were divided into control group and SEV group two subgroups, the control group no longer any treatment, the SEV group access to 5.1% SEV, 15min after given different concentrations of Ang Ⅱ, each vascular segment only randomized to a single Dose AngⅡ stimulation to measure the peak level of vasoconstrictor response. The second part: The vascular segments were immersed in KBS containing 10-4mol / L N-L-NAME for 15min, and then were given 10-7mol / LAngII to measure the vasoconstrictive response Peak. The third part: The two vascular segments were immersed in KBS with different SEV concentrations (0,1.7%, 3.4% and 5.1%) for 15min and then given 10-7mol / LAngII to observe the effect of SEV on AngⅡ-induced vasoconstriction Inhibit effect. Results The first part: compared with the control group, the aortic contractile responses of SEV group were decreased in the normal and endometrial groups when the concentrations of AngⅡ were 3 × 10-8-10-6 mol / L and 3 × 10-9-10-6 mol / L, respectively (P <0.05 or 0.01). Compared with the normal group, the aortic contractile response in SEV group was significantly increased at the concentration of 3 × 10-9-10-6 mol / L (P <0.05 or 0.01) . The second part: The Ang Ⅱ-induced contraction of vascular segments in the normal group increased from 43% ± 5% without L-NAME to 71% ± 6% (P <0.01) with L-NAME treatment; Vascular segment contractile response without and without L-NAME treatment group did not change. The third part: the aortic contractile response of endomembrane group was higher than that of the normal group (P <0.05) when the SEV concentration was 0-5.1%; compared with the SEV concentration of 0, the SEV concentration of the normal group was 3.4% and 5.1 Aortic contractions were reduced at%, and aortic contractions were reduced at SEV concentrations of 1.7% -5.1% in the endometrial group (P <0.05 or 0.01). Conclusion SEV can inhibit the contraction induced by angiotensin Ⅱ in a dose-dependent rat aorta, and can inhibit the inhibition of vascular intima; SEV can also inhibit the vasodilatation induced by AngⅡ in endometrium.