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  • Title: [Effects of high pulmonary blood flow on pulmonary vascular structure and the gene expression of cystathionine-gamma-lyase].
    Author: Shi L, Du J, Pu D, Qi J, Wei B, Tang C, Tang X.
    Journal: Beijing Da Xue Xue Bao Yi Xue Ban; 2003 Dec 18; 35(6):566-70. PubMed ID: 14710245.
    Abstract:
    OBJECTIVE: To examine the alteration of pathologic structure and endogenous hydrogen sulfide pathway in rats with pulmonary hypertension induced by high pulmonary blood flow. METHODS: Sixteen SD rats were randomly divided into shunting group and control group. An 11-week aortocaval shunting was produced in rats of shunting group, and pulmonary artery mean pressure (mPAP) was evaluated using right cardiac catheterization. The ratios of right ventricular mass to body weight (RV/BW) and right ventricular mass to left ventricular plus septal mass [RV/(LV+S)] were also detected. Pulmonary vascular micro- and ultra- structures were examined. Meanwhile the concentration of plasma hydrogen sulfide (H(2)S) was measured by spectrophotography. The gene expression of cystathionine-gamma-lyase (CSE)was detected by in situ hybridization, and the activity of CSE in lung tissues was measured by H(2)S production according to chemical analysis. RESULTS After 11 weeks of aortocaval shunting, pulmonary artery mean pressure was significantly increased. Muscularization of small pulmonary vessels and relative medial thickness of pulmonary arteries were obviously increased in shunting rats compared with controls. Ultrastructure of intrapulmonary arteries changed obviously in shunting rats. Meanwhile, plasma H(2)S concentration was decreased and the activity of CSE (according to H(2)S production) in lung tissues decreased in shunting rats. CSEmRNA expression by pulmonary arteries was significantly suppressed. CONCLUSION: Pulmonary vascular structural remodeling is the important pathologic basis for pulmonary hypertension induced by high pulmonary blood flow. The down-regulation of endogenous H(2)S pathway might play an important role in the development of high pulmonary blood flow induced pulmonary hypertension.
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