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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 2S) was measured by spectrophotography. The gene expression of cystathionine ? lyase (CSE)was detected by in situ hybridization, and the activity of CSE in lung tissues was measured by H 2S 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 2S concentration was decreased and the activity of CSE (according to H 2S 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 regula tion of endogenous H 2S pathway might play an im portant role in the development of high pulmonary blood flow induced pulmonary hypertension.
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Objective To investigate the changes of Toll-like receptor 2 and 4 gene expression in lungs with acute injury induced by acute hemorrhagic necrotizing pancreatitis(AHNP) in rats.Methods Forty SD male rats were randomly divided into sham-operated group(n=10),and AHNP group(n=30).Of all the rats,the lungs were dissected for lung histological scores and bronchoalveolar lavages were harvested for lung injury index.TLR2,4mRNA expression in the lungs was measured by RT-PCR at different time points.(Results) TLR2,4mRNA could be detected in lungs with low values in sham-operated group;but they were markedly increased at 3 hours in AHNP group,peaking at 6~12 hours(P
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Objective To investigate the effect of MMP-9 on severe acute pancreatitis(SAP) associated with lung injury,and the preventive function of MMP-9 inhibitor (BB-94) in SAP associated with lung injury in rats. Methods SD rats were randomly divided into three groups: Shamed-operated groups (control groups,n=10);SAP groups (n=14);SAP with MMP-9 inhibitor preconditioning groups (BB-94 group,n=15). The samples for test of the wet weigh index of lung,serum amylase level,white cell count,the number of cells and protein in bronchoalveolus lavage fluid,histologic scoring of lung injury and MMP-9 in lung were detected 24 hours after SAP models were set up.Results The parameters mentioned above in SAP group were significant higher than those in controll group and BB-94 group (P
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Objective To study the pathological changes of acute hemorrhagic necrotizing pancreatitis(AHNP) complicated with acute lung injury(ALI). Method The model of AHNP with ALI was established in rats. The changes of function and structure of pancreas and lung were observed. Results One hour after induction of the model , pancreas showed mild edema and congestion . 12 hours after introduction of the model , the typical pathological changs of AHNP were found . The lung extravascular water volume and levels of PaCO 2 increased significantly, and the PaCO 2 decreased obviously. Morphological examination demonstrated that inflammatory cell , insterstitial edema , intra-alveolar hemorrhage ,desquamate and disintegration occurred in the lungs. Conclusions The pancreatic and pulmonary morphologic changes in this model is similar to the changes in clinical AHNP with ALI , which suggests that the model can be used to study the mechanism of AHNP with ALI and evaluate the effect of drugs for AHNP with ALI.