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目的探讨腺苷通过外周途径持续给药能否拮抗大鼠慢性缺氧引起的右心肥厚和肺动脉高压(PAH)及其间的量效关系。方法将48只SD大鼠随机分为缺氧组(n=6)、缺氧腺苷治疗组[n=18,按剂量分为3组,分别为50、100、150μg/(kg.min),即缺氧腺苷治疗A、B、C组]、对照组(n=6)、腺苷治疗对照组[n=18,按剂量分3组,分别为50、100、150μg/(kg.min),即正常腺苷治疗A、B、C组]。于实验的第21天,测定每只大鼠的右室收缩压(RVSP)、平均肺动脉压(mPAP)及右心室/(左心室加室间隔)[RV/(LV+S)]、右心室/体质量(RV/BW)的比值。进一步行右心室及右下肺叶组织病理切片,观察其形态学变化。采用SAS8.0软件进行统计学分析。结果缺氧组RVSP、mPAP、RV/(LV+S)及RV/BW均显著高于对照组(Pa<0.01),而缺氧腺苷治疗组的上述指标显著低于缺氧组(Pa<0.01),但与对照组比较均有统计学差异(Pa<0.05)。腺苷剂量为150μg/(kg.min)时的抗肥厚效果最好。腺苷剂量为50μg/(kg.min)时能降低正常大鼠的RVSP及mPAP(Pa<0.05)。结论腺苷通过外周途径持续给药能拮抗大鼠缺氧引起的右心肥厚和PAH,且存在一定的量效关系。
Objective To investigate whether continuous administration of adenosine through the peripheral pathway can antagonize right ventricular hypertrophy and pulmonary hypertension (PAH) caused by chronic hypoxia in rats and their dose-response relationship. Methods 48 SD rats were randomly divided into three groups: hypoxia group (n = 6) and hypoxia group (n = 18). The rats were divided into three groups according to dosage: 50,100,150μg / (kg · min) (A, B and C), control group (n = 6) and adenosine control group (n = 18). The doses were divided into three groups, 50,100,150μg / (kg. min), that is, normal adenosine A, B, C group]. On day 21 of the experiment, RVSP, mPAP, and RV / LV / RV were measured in each rat. The right ventricle / Body mass (RV / BW) ratio. Further line the right ventricle and right lower lobe histopathology, to observe the morphological changes. SAS8.0 software was used for statistical analysis. Results The levels of RVSP, mPAP, RV / (LV + S) and RV / BW in hypoxia group were significantly higher than those in control group (P <0.01), while those in hypoxia group were significantly lower than those in hypoxia group 0.01), but compared with the control group were statistically significant (Pa <0.05). Adenosine dose of 150μg / (kg.min) when the best anti-hypertrophy effect. Adenosine dose of 50μg / (kg.min) can reduce RVSP and mPAP in normal rats (Pa <0.05). Conclusion Continuous administration of adenosine through the peripheral pathway can antagonize hypoxia-induced right ventricular hypertrophy and PAH, and there is a certain dose-effect relationship.