AIM:To investigate the role of potassium channel expression alteration in chronic cigarette smoking-induced increase in pulmonary vascular responsiveness,the effect of chronic cigarette smoking on large-conductance calcium-activated potassium channel(BKCa) and voltage-dependent delayed rectifier potassium channel(Kv1.5) expression in rat pulmonary smooth muscle cells were investigated in vivo.METHODS: HE staining,immuno-histochemistry and in situ hybridization techniques were used.RESULTS:(1) Chronic cigarette smoking downregulates the protein and mRNA expression of BKCa in pulmonary arterial smooth muscles.(2) Chronic cigarette smoking downregulated the protein and mRNA expression of Kv1.5 in pulmonary arterial smooth muscles.(3) In big artery,BKCa decreased more makedly than Kv1.5,but in small artery,both of them decreased equally.CONCLUSION: Chronic cigarette smoking downregulates the levels of BKCa and Kv1.5 in rat pulmonary arterial smooth muscle cells in vivo,which maybe contribute to the mechanism of cigarette smoking-induced increase in pulmonary vascular responsiveness.

AIM: To investigate the role of Ca2+ - activated, delayed - rectifier and ATP sensitive K+ channel (KCa, Kdr, KATP) in airway hyperresponsiveness of asthmatic guinea pigs. METHODS: The method of recording the tone of isolated trachea rings was performed, and the changes of dose-response curves of trachea rings to histamine caused by different K+ channel blockade were investigated. RESULTS: (1) After inhibition of KCa, by tetraethylammonium (TEA) , the dose - response curve of trachea rings to histamine did not change in control group, while the maximal contraction of trachea rings to 10-4 mol/L and 10-3 mol/L histamine decreased significantly ( P < 0.01) and dose-response curve shifted down significantly in asthmatic group. (2) After inhibition of Kdr. by 4 - aminopyridine (4 - AP), the maximal contraction to 10-3 mol/L histamine decreased ( P < 0.05) and dose - response curve shifted down in control group, the response to 10-4 mol/L and 10-3 mol/L histamine decreased significantly (P < 0.01) and dose - response curve shifted down more significantly in asthmatic group and the decrease of the latter was more significant than that in control group ( P < 0.05) ; (3) The dose-response curves did not change by KATp blocker glibenclamide (Glib) in both control and asthmatic group. CONCLUSION: The depression of both KCa and Kdr might mediate the airway hyperresponsiveness in asthmatic guinea pigs, whereas the KATP doesn't take part in it.

Hypoxia is a commenest pathological process. The cellular oxygen sensors and signal transduction involved in hypoxic responses are so far not fully elucidated. There are many theories. Perhaps the oxygen sensors are different among different kinds of cells, and between acute and chronic hypoxic responses. The mitochondria cytochrom-oxidase-H_2O_2 might be the principal pathway leading to the constrictive response of pulmonary smooth muscle cells to hypoxia. The heme protein - reactive oxygen pathway might mediate the response of glomus cells in carotid body to hypoxia. The NADPH oxidase might be the oxygen sensor in airway chemoreceptor. As for chronic hypoxic responses, the oxygen dependent regulation of hypoxia-inducible factors by prolyl and asparaginyl hydroxylation has been paid great attention in recent years.

华中科技大学同济医学院病理生理学系开展了病理生理学与临床相结合途径与方法的探讨和实践,如大课强化临床病例教学,并请临床教授讲授部分大课,学生跟随临床教师查房等.研究结果显示,改革班成绩高于对照班,学生学习兴趣大大提高.病理生理学与临床相结合的途径与方法,是有效可行的.