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观察外源性腺苷对正常大鼠血流动力学的影响及可能的作用机制。方法 :从正常大鼠肺动脉内注入不同浓度的腺苷溶液或等量的生理盐水 ,持续 15分钟。结果 :2 5 μg/ (kg· min)组 (T组 )、5 0 μg/ (kg· min)组 (F组 )、10 0 μg/ (kg· m in)组 (H组 )大鼠用药后平均肺动脉压 (m PAP)分别增高 2 0 .6 %± 10 .0 %、33.8%± 18.7%、40 .4%± 17.6 % ,高于用药前 (P<0 .0 5、0 .0 5、0 .0 1) ,与生理盐水组 (S组 )比较 ,差异有显著性 (P<0 .0 5、0 .0 5、0 .0 1) ,T、F、H、S组用药前后平均体循环压 (m SAP)、TXB2 、6 - keto- PGF1 a、NO的水平及心率均无明显改变。结论 :腺苷引起正常大鼠肺动脉压剂量依赖性升高 ,其机制可能不通过环氧化酶代谢产物或 NO的途径。
To observe the effect of exogenous adenosine on hemodynamics in normal rats and its possible mechanism. Methods: Different concentrations of adenosine solution or normal saline were injected into the pulmonary artery of normal rats for 15 minutes. Results: The rats in the 25 μg / (kg · min) group (T group), 50 μg / (kg · min) group (F group), and 10 μg / (kg · mint) The mean pulmonary artery pressure (m PAP) increased by 20.6% ± 10.0%, 33.8% ± 18.7% and 40.4% ± 17.6%, respectively, which was higher than that before treatment (P <0.05, 5,0. 01), compared with the saline group (S group), the difference was significant (P <0.05, 0.050,0.01), T, F, H, S group Before and after the mean body mass pressure (m SAP), TXB2, 6 - keto - PGF1 a, NO levels and heart rate did not change significantly. CONCLUSION: Adenosine causes a dose-dependent increase in pulmonary arterial pressure in normal rats, and its mechanism may not be through the pathway of cyclooxygenase metabolites or NO.