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作 者:杜军保[1,2] 赵斌[1,2] 黎文 李万镇[1,2]
机构地区:[1]北京医科大学第一医院儿科 [2]北京积水潭医院
出 处:《中华儿科杂志》1998年第1期19-21,共3页Chinese Journal of Pediatrics
基 金:国家自然科学基金;卫生部全国优秀青年科技人才专项基金
摘 要:目的探讨一氧化氮体系在缺氧性肺动脉高压形成机制中的作用。方法采用地高辛精标记的一氧化氮合酶(NOS)cRNA探针对缺氧组大鼠(6只)及对照组大鼠(7只)进行原位杂交。结果缺氧2周后的大鼠肺动脉收缩压(3.8±0.7kPa)(28±5mmHg,1kPa=7.5mmHg)、肺动脉平均压(2.8±0.6kPa)及肺动脉舒张压(1.4±0.4kPa)与对照组(2.9±0.5kPa,1.9±0.5kPa及0.9±0.5kPa)相比均显著升高。缺氧组大鼠肺动脉内皮细胞中NOSmRNA表达信号为弱阳性(3只)及阴性(3只),平滑肌细胞中表达信号均为阴性;对照组大鼠肺动脉内皮细胞中NOSmRNA表达信号为阳性(7只),平滑肌细胞中表达信号均为阴性。NOSmRNA的表达强度与大鼠肺动脉收缩压、肺动脉平均压及肺动脉舒张压分别呈负相关(rs=-0.673、-0.596及-0.621,P均<0.05)。结论缺氧时肺动脉内皮细胞NOSmRNA表达的改变可能参与慢性缺氧性肺动脉高压的形成。Objective To explore the possible role of nitric oxide (NO) system in the development of hypoxic pulmonary hypertension. Methods The investigators used in situ hybridization (ISH) and employed digoxigenin labelled cRNA probe for NO synthase (NOS) mRNA to detect the changes in NOS mRNA expression in pulmonary arteries of hypoxic pulmonary hypertensive rats. Lung sections of 6 hypoxic rats and of 7 control rats were used for ISH. Results Pulmonary artery systolic pressure (PASP), pulmonary artery mean pressure (PAMP) and pulmonary artery diastolic pressure (PADP) were significantly elevated in hypoxic rats compared with controls, respectively (3.8±0.7 kPa vs. 2.9± 0.5 kPa, 2.8±0.6 kPa vs. 1.9±0.5 kPa and 1.4±0.4 kPa vs. 0.9±0.5 kPa, respectively). All lung sections of normoxic rats showed NOS mRNA positive expression by endothelial cells of pulmonary arteries, whereas only 3/6 sections of hypoxic rats showed NOS mRNA weak signals and the other 3/6 negative. The intensity of the expression of NOS gene by endothelial cells of pulmonary arteries was negatively correlated to PASP, PAMP and PADP, respectively ( r s =-0.673, -0.569 and -0.621, respectively, P all< 0.05). Conclusion Alteration in NOS mRNA expression by endothelial cells of pulmonary arteries is probably involved in the mechanisms of hypoxic pulmonary hypertension.
分 类 号:R543.202[医药卫生—心血管疾病]
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