ObjectiveTo explore effect of α-adrenoceptor on modulating water of lung in severe acute pancrea-titis (SAP) rat. MethodsThe SD rats were randomly divided into sham operation group (n=5) and SAP group,the SAP group was divided into subgroups of SAP-4 h (n=5) and SAP-24 h (n=5).SAP model was made by injecting taurocholate into bilopancreatic duct.The wet-to-dry ratio,alveolar fluid clearance (AFC),and AFC affected by α1-adrenoceptor inhibitor-prazosin and α2-adrenoceptor inhibitor-yohimbine separately or together were measured in the lungs.The α1-adrenoceptor and α2-adrenoceptor mRNA expressions in the lungs tissues were measured by real-time PCR. Results① The wet-to-dry ratios in the SAP-4 h group and SAP-24 h group were obviously decreased as compared with the sham operation group (P<0.05),which in the SAP-24 h group was significantly lower than that in the SAP-4 h group (P<0.05).② The AFCs in the SAP-4 h group and SAP-24 h group were obviously increased as compared with the sham operation group (P<0.05).The AFCs in the SAP with α1-adrenoceptor inhibitor-prazosin or α2-adrenocpetor inhibitor-yohimbine or prazosin combined with yohimbine were all obviously decreased as compared with the SAP group (P<0.05).③ The α1 adrenoceptor and α2 adrenoceptor mRNAs in the SAP-4 h group and SAP-24 h group were obviously increased as compared with the sham operation group (P<0.05). ConclusionAFC might be modulated by α-adrenoceptor in SAP rat.
Objective To investigate the influence of hypoxic preconditioning on pulmonary structure of rats exposed to simulated high altitude hypoxia and to explore the role of hypoxia inducible factor-1α(HIF-1α).Methods Fifty-six Wistar rats were randomly divided into 7 groups(n=8 in each group),ie,a normal control group(N group),an acute hypoxic control group(H0 group),an acute hypoxic group(H1 group),a 3 000 m hypoxic preconditioning group(C3.0 group),a 3 000 m hypoxic preconditioning + acute hypoxic group (C3.1 group),a 5 000 m hypoxic preconditioning group(C5.0 group),and a 5 000 m hypoxic preconditioning + acute hypoxic group(C5.1 group).After treated with hypoxic preconditioning,the animals were exposed to simulated altitude of 6 000 m for 24 hours.Then the protein and mRNA expression of HIF-1α in lung of N,H0,C3.0 and C5.0 groups were assessed by Western blot and RT-PCR,respectively.The lung structure in N,H1,C3.1 and C5.1 groups was observed by light microscope and electron microscope.Results Pulmonary interstitial edema was apparently observed in H1 group,while significantly relieved in two hypoxic preconditioning groups.HIF-1α protein was not detected in rat lungs by Western blot analysis.Compared to N group,the levels of HIF-1α mRNA significantly increased in C3.0 group and C5.0 group(both Plt;0.01).Conclusions Hypoxic preconditioning can relieve hypoxic pulmonary interstitial edema and increase HIF-1α mRNA expression in rat lungs.HIF-1 may be involved in the process of hypoxic preconditioning in rat lungs.
ObjectiveTo discuss the effect ofβ2 adrenoceptor on the alveolar fluid clearance (AFC) of the rats with severe acute pancreatitis (SAP). MethodsSD rats was made to SAP model by injecting taurocholate into biliary-pancreatic duct.These rats were randomly divided into sham operation group and SAP group, the SAP group was divided into subgroups of SAP-4 h and SAP-24 h according to the sampling time after making model.The wet-to-dry ratio, AFC, and AFC affected byβ2 adrenoceptor agonist-terbutaline or inhibitor-propranolol were measured in the bilateral lungs.β2 adrenoceptor mRNA expression in the lungs tissues was measured by real-time-PCR. ResultsCompared with the sham operation group, the wet-to-dry ratio was significantly decreased (P < 0.05) and the AFC was significantly increased in the subgroup of SAP-4 h or SAP-24 h (P < 0.05), β2 adrenoceptor agonist-terbutaline couldn't increase the AFC of the subgroup of SAP-4 h or SAP-24 h (P > 0.05), inhibitor-propranolol could decrease AFC of subgroup of SAP-4 h or SAP-24 h (P < 0.05).β2 adrenoceptor mRNA was decreased in the subgroup of SAP-4 h or SAP-24 h as compared with the sham operation group (P < 0.05). ConclusionsBilateral lung liquid volome induced by SAP is less than the normal lung, AFC is increased in the early period of SAP but decreased in the late period.when the lung injury happens, β2 adrenoceptor might modulate AFC in rats of SAP model.The mechanism of lung injury of SAP is so complex that we need more experiments to be done.
【摘要】 目的 探讨腹水引起的腹内高压对肝硬化小鼠肺组织水通道蛋白1(AQP1)和水通道蛋白5(AQP5)表达的影响。 方法 雄性美国癌症研究所(Institudo of Cancer Reseach,ICR)小鼠50只,随机取10只作正常对照组(腹压0 cm H2O,1 cm H2O=0.098 kPa),其余40只用四氯化碳建立肝硬化小鼠模型,并随机分为4组:肝硬化(腹压0 cm H2O)组、肝硬化(腹压5 cm H2O)组、肝硬化(腹压10 cm H2O)组、肝硬化(腹压20 cm H2O)组,通过腹腔注射不同量的白蛋白生理盐水形成不同的腹压,并维持腹压24 h后取肺组织行病理、免疫组织化学、肺湿/干比值及实时荧光定量PCR检测AQP1和AQP5 mRNA表达量。 结果 与正常对照小鼠相比,肝硬化小鼠肺AQP5、AQP1表达明显下降(Plt;0.05);肝硬化小鼠随着腹内压的升高,肺湿/干比值升高,AQP5、AQP1表达相应增加(Plt;0.05)。 结论 肝硬化可以影响肺AQP1、AQP5的表达;肝硬化小鼠随着腹内压的升高,AQP1、AQP5表达相应增加,并与肺水肿的严重程度密切相关。【Abstract】 Objective To investigate the role of intra-abdominal hypertension caused by ascites on the expression of Aquaporin (AQP) 1 and AQP 5 in the lung of cirrhotic mice. Methods We randomly chose 10 from 50 male Institude of Cancer Research (ICR) mice to form the control group [intra-abdominal pressure (IAP)=0 cm H2O, 1 cm H2O=0.098 kPa]. The model of cirrhosis were prepared by subcutaneous injection of carbon tetrachloride for the rest 40 mice which were then randomly divided into 4 groups: cirrhosis (IAP=0 cm H2O) group, cirrhosis (IAP=5 cm H2O) group, cirrhosis (IAP=10 cm H2O) group, and cirrhosis (IAP=20 cm H2O) group. Saline with different volume of albumin was injected into the peritoneum of each mouse in order to form different IAP. After 24 hours, analysis of pathology, immunochemistry and wet/dry ratio was done for the lungs of these mice; and the expression of AQP1 and AQP5 at the protein and mRNA levels were analyzed by IHC and qRT-PCR. Results Compared with the normal mice, the expression of AQP1 and AQP5 in lungs of cirrhotic mice were significantly lower (Plt;0.05). Both the lung wet/dry ratio and the expression of AQP1 and AQP5 raised with the increase of IAP. Conclusion Cirrhosis can affect the expression of AQP1 and AQP5 in lungs. The expression of AQP5 and AQP1 in lungs of cirrhotic mice increases with the increase of IAP, which is also closely correlated with the severity of pulmonary edema.