首页 | 本学科首页   官方微博 | 高级检索  
检索        

缓激肽介导的治疗心血管和糖尿病药物致血管性水肿的研究进展
引用本文:刘玉龙,舒冰.缓激肽介导的治疗心血管和糖尿病药物致血管性水肿的研究进展[J].中国现代应用药学,2020,37(22):2810-2816.
作者姓名:刘玉龙  舒冰
作者单位:安徽医科大学附属妇幼保健院,安徽医科大学附属妇幼保健院,安徽医科大学附属妇幼保健院
基金项目:国家自然科学基金项目(面上项目,重点项目,重大项目)
摘    要:目的 本研究旨在调查慢性射血分数降低的心力衰竭(HFrEF)患者神经内分泌抑制剂-血管紧张素转换酶抑制剂(ACEI)或血管紧张素II受体阻滞剂(ARB)、β受体阻滞剂(BB)和醛固酮受体拮抗剂(MRA)使用现状及其与指南的差距。方法 搜集并分析2018年01月到12月HFrEF住院患者基本资料和三类神经内分泌抑制剂使用情况。结果 共纳入301例慢性HFrEF患者,平均年龄为71.3±11岁,男性占56.5%,平均EF值32.1±7.2%,51.8%合并有高血压,心衰最常见的病因是心脏瓣膜病。ACEI/ARB、BB和MRA使用率分别为77.4%,60.5%和94.0%,剂量达标率分别为44.2%、22.5%和100%。48.8%患者采用指南推荐的联合用药,包括1.3%两药联合(ACEI/ARB+BB)和47.4%三药联合(ACEI/ARB+ BB+MRA)。结论 该院慢性HFrEF患者神经内分泌抑制剂应用现状与指南仍有差异,ACEI/ARB和BB使用率和剂量达标率不足,而MRA使用过度,需进一步提高医生对指南依从性。

关 键 词:心力衰竭  血管紧张素转换酶抑制剂  血管紧张素II受体阻滞剂  β受体阻滞剂  醛固酮受体拮抗剂
收稿时间:2020/1/17 0:00:00
修稿时间:2020/3/27 0:00:00

Advances in the Bradykinin-mediated Angioedema Caused by Cardiovascular and Diabetic Medications
LIU Yulong,SHU Bing.Advances in the Bradykinin-mediated Angioedema Caused by Cardiovascular and Diabetic Medications[J].The Chinese Journal of Modern Applied Pharmacy,2020,37(22):2810-2816.
Authors:LIU Yulong  SHU Bing
Institution:Anhui Women and Child Health Care Hospital Affiliated to Anhui Medical university,Anhui Women and Child Health Care Hospital Affiliated to Anhui Medical university,Anhui Women and Child Health Care Hospital Affiliated to Anhui Medical university
Abstract:Objective: To study the effect of saponins from panaxjaponicus (SPJ) on the sensitivity of cisplatin resistant lung cancer cells and its potential mechanism. Methods: Drug resistance of lung cancer A549 cells was induced by increasing concentration, drug sensitivity was determined by SRB colorimetry, Annexin V- FITC/PI double staining assay was used to detect apoptosis, Caspase 3 and Caspase 8 levels was determinate by ELISA and the expression of related proteins in cells was determined by Western blot. Results: After long-term induction, the tolerance of A549 cells to cisplatin was increased by 14.79 times and was relatively stable. Compared with cisplatin treatment group, the combination of SPJ and cisplatin could significantly increase the sensitivity of A549 cells to cisplatin, increase intracellular Caspase 3 and Caspase 8 levels and promote apoptosis. At the same time, the expression of MDR1, P-gp, Bcl-2 and P-Akt was inhibited, and the expression of Bax protein was promoted. Conclusion: SPJ could increase the sensitivity of cisplatin-resistant cell lines to cisplatin and enhance the effect of cisplatin, which mechanism might be through inhibiting the activity of drug-resistant related proteins MDR1, P-gp and Akt.
Keywords:Heart failure  Angiotensin converting enzyme inhibitor  Angiotensin II receptor blocker  Beta-blocker  Mineralocorticoid receptor antagonist
点击此处可从《中国现代应用药学》浏览原始摘要信息
点击此处可从《中国现代应用药学》下载免费的PDF全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号