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作 者:李晓惠[1] 杜军保[1] 金红芳[1] 丁亚光[1] 卜定芳[2] 李简[3] 唐朝枢[4]
机构地区:[1]北京大学第一医院儿科,北京100034 [2]北京大学第一医院中心实验室,北京100034 [3]北京大学第一医院胸外科,北京100034 [4]北京大学第一医院心血管病研究所分子心血管学教育部重点实验室,北京100034
出 处:《中国应用生理学杂志》2007年第1期75-79,共5页Chinese Journal of Applied Physiology
基 金:国家杰出青年科学基金(30425010);北京市自然科学基金(7052043);国家重点基础研究发展规划课题(2006CB503807)
摘 要:目的:探讨大鼠早期高肺血流性肺动脉高压形成中内源性硫化氢体系的动态变化规律。方法:雄性SD大鼠80只,体重140~160g,随机分为分流组(40只)和对照组(40只)。分流组大鼠经下腔静脉一腹主动脉穿刺术建立高肺血流动物模型。分别在术后1d、3d、1周、4周及8周各实验时间点测量肺动脉收缩压(SPAP)、肺组织匀浆中硫化氢(H,S)含量及CASEmRNA相对含量。结果:sPAP于分流后1周开始升高,8周明显升高;肺组织H2S及CASEmRNA含量于分流后3d及4周显著升高;SPAP与肺组织H2S、CSEmRNA含量于分流后1周、4周及8周呈明显负相关。结论:大鼠高肺血流性动物模型可导致肺动脉高压,早期伴随内源性肺组织H2S及CSEmRNA含量的变化,提示内源性H2S体系可能与高肺血流性肺动脉高压形成有关,并在其中发挥保护性的调节作用。Aim: To explore the time-dependent changes of endogenous hydrogen sulfide system at the early stage of pulmonary hypertension induced by high pulmonary flow in rats. Methods: Eighty male SD rats, whose weight ranged 140-160 g, were randomly divided into control group ( n = 40) and shunt group ( n = 40). Rats in shunt group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. After 1 d, 3 d, 1 week, 4 week and 8 weeks of experiment, systolic pulmonary artery pressure (SPA.P) of each rat, the H2S of rat lung tissue and CSErnRNA of rat lung tissue were evaluated, respectively. Results: SPAP increased significantly as compared with those in control group in 1 week and 8 weeks of experiment. In contrast to control group, the H2S of rat lung tissue increased significantly on 3 d and in 4 weeks, respectively. Meanwhile, in contrast to control group, relative amount of CSE mRNA of lung tissues elevated significantly on 3 d and in 4 weeks, respectively. Moreover, SPAP and the H2S of rat lung tissue, the CSE mRNA of rat lung tissue correlated negatively in 1 week, 4 weeks and 8 weeks, of experiment. Conclusion: Animal model of rats with high pulmonary bkx)d flow exhibited pulmonary hypertension. Lung tissue H2S and CSE mRNA of rats exhibited double peaks within 8 weeks. These results revealed that endogenous H2S system might be relevant with the development of pulmonary hypertension induced by high pulmonary blood flow, and probably, it played a protective role in the regulation of pulmonary hypertension, especially, at its early stage.
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