Background Chronic hypoxia can cause pulmonary hypertension and pulmonary heart disease with high mortality.The signal transduction pathway of protein kinase C (PKC) plays an important role in chronic pulmonary hype...Background Chronic hypoxia can cause pulmonary hypertension and pulmonary heart disease with high mortality.The signal transduction pathway of protein kinase C (PKC) plays an important role in chronic pulmonary hypertension. So it is necessary to investigate the effect of PKC on voltage-gated potassium (K +) channels in pulmonary artery smooth muscle cells of rats exposed to chronic hypoxia. Methods Male Wistar rats were randomly divided into a control group (group A) and a chronic hypoxia group (group B). Group B received hypoxia [oxygen concentration (10±1)%] eight hours per day for four consecutive weeks. Single pulmonary artery smooth muscle cells were obtained using an acute enzyme separation method. Conventional whole cell patch clamp technique was used to record resting membrane potential,membrane capacitance and voltage-gated K + currents. The changes in voltage-gated K + currents before and after applying paramethoxyamphetamine (PMA) (500 nmol/L),an agonist of PKC,and PMA plus carbohydrate mixture of glucose,fructose and xylitol (GFX) (30 nmol/L),an inhibitor of PKC,were compared between the two groups. Results The resting membrane potential in group B was significantly lower than that of group A: -(29.0±4.8) mV (n=18) vs -(42.5±4.6) mV (n=35) ( P <0.01). But there was no change in membrane capacitance between the two groups: (17.9±4.6) pF (n=40) vs (19.7±5.8) pF (n=31) ( P >0.05). The voltage-gated K + currents were significantly inhibited by PMA in group A,and this effect was reversed by GFX. However,the voltage-gated K + currents in group B were not affected by PMA. Conclusions The resting membrane potential and voltage-gated K + currents in pulmonary artery smooth muscle cells from rats exposed to chronic hypoxia decreased significantly. It seems that PKC has different effects on the voltage-gated K + currents of pulmonary artery smooth muscle cells under different conditions.展开更多
基金ThisworkwassupportedbyagrantfromtheNationalNaturalScienceFoundationofChina (No 3 9970 3 3 2 )
文摘Background Chronic hypoxia can cause pulmonary hypertension and pulmonary heart disease with high mortality.The signal transduction pathway of protein kinase C (PKC) plays an important role in chronic pulmonary hypertension. So it is necessary to investigate the effect of PKC on voltage-gated potassium (K +) channels in pulmonary artery smooth muscle cells of rats exposed to chronic hypoxia. Methods Male Wistar rats were randomly divided into a control group (group A) and a chronic hypoxia group (group B). Group B received hypoxia [oxygen concentration (10±1)%] eight hours per day for four consecutive weeks. Single pulmonary artery smooth muscle cells were obtained using an acute enzyme separation method. Conventional whole cell patch clamp technique was used to record resting membrane potential,membrane capacitance and voltage-gated K + currents. The changes in voltage-gated K + currents before and after applying paramethoxyamphetamine (PMA) (500 nmol/L),an agonist of PKC,and PMA plus carbohydrate mixture of glucose,fructose and xylitol (GFX) (30 nmol/L),an inhibitor of PKC,were compared between the two groups. Results The resting membrane potential in group B was significantly lower than that of group A: -(29.0±4.8) mV (n=18) vs -(42.5±4.6) mV (n=35) ( P <0.01). But there was no change in membrane capacitance between the two groups: (17.9±4.6) pF (n=40) vs (19.7±5.8) pF (n=31) ( P >0.05). The voltage-gated K + currents were significantly inhibited by PMA in group A,and this effect was reversed by GFX. However,the voltage-gated K + currents in group B were not affected by PMA. Conclusions The resting membrane potential and voltage-gated K + currents in pulmonary artery smooth muscle cells from rats exposed to chronic hypoxia decreased significantly. It seems that PKC has different effects on the voltage-gated K + currents of pulmonary artery smooth muscle cells under different conditions.
文摘目的分析新森林父母培训方案(new forest parenting programme,NFPP)对注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)儿童及家庭的干预效能,探索该方案在中国实施的可行性和有效性。方法纳入2022年1月至2023年5月就诊于暨南大学附属第一医院儿童心理发育行为门诊确诊的22例ADHD儿童及其22例亲密养育人,根据亲密养育人的个人意愿分为试验组(n=11)和对照组(n=11),对试验组进行每周1次、为期8周的NFPP干预。采用中文版注意缺陷多动障碍SNAP-Ⅳ评定量表(Chinese version of Swanson Nolan and Pelham,versionⅣscale-parent form,SNAP-Ⅳ)、Weiss功能缺陷评定量表父母版(Weiss functional impairment rating scales-parent report,WFIRS-P)评估试验组和对照组在干预前后核心症状及社会功能损害的改善情况。试验组采用中文版父母养育胜任感评定量表(China parenting sense of competence scale,C-PSOC)、育儿方式和维度问卷(parenting styles and dimensions questionnaire,PSDQ)评估NFPP干预前后ADHD家庭亲密养育人的育儿效能和育儿方式的改善情况。干预结束后对试验组的11例ADHD儿童的亲密养育人进行关于ADHD疾病诊疗相关知识、养育态度及事实养育行为的半开放性访谈。使用SPSS 26.0分析数据,采用独立样本t检验、配对样本t检验、Mann-Whitney U检验和秩和检验进行统计分析。结果(1)干预后,试验组SNAP-Ⅳ量表总分[(4.01±1.05)分,(2.79±0.94)分;t=2.875,P<0.05]、对立违抗分量表评分[(1.27±0.34)分,(0.70±0.33)分;t=4.043,P<0.05]、WFIRS-P的家庭[(0.92±0.47)分,(0.56±0.26)分;t=2.246,P<0.05]和生活技能维度评分[1.1(0.9,1.3)分,0.6(0.5,0.8)分;Z=-2.013,P<0.05]均低于对照组。干预后,试验组SNAP-IV量表中注意缺陷、冲动/多动、对立违抗3个维度和SNAP-IV总分的评分均较干预前显著降低(均P<0.05)。(2)干预后,试验组C-PSOC量表中育儿效能感维度评分较干预前显著升高(P<0.05);干预后,
