目的：观察微量泵持续注射硝普钠与多巴胺治疗顽固性心衰的临床疗效。方法：选择106例心功能Ⅲ-Ⅳ级顽固性心衰患者,采用微量泵持续泵入硝普钠和多巴胺进行顽固性心衰治疗,硝普钠起始剂量为6.25μg/min;同时采用另一微量泵持续泵入多巴...目的：观察微量泵持续注射硝普钠与多巴胺治疗顽固性心衰的临床疗效。方法：选择106例心功能Ⅲ-Ⅳ级顽固性心衰患者,采用微量泵持续泵入硝普钠和多巴胺进行顽固性心衰治疗,硝普钠起始剂量为6.25μg/min;同时采用另一微量泵持续泵入多巴胺,起始剂量为2 g/kg·min,直至血压下降至90-100 mm Hg;连续用药7 d,观察治疗后患者症状体征和心功能各参数的变化情况。结果：1106例顽固性心衰患者经硝普钠与多巴胺微泵治疗后,总有效率为85.85%（91/106）;2微量泵治疗后顽固性心衰患者的心率、血压、心胸比率、左室短轴缩短率、每搏输出量、每搏指数以及左室射血分数等参数较治疗前均有明显改善。结论：微量泵持续注射硝普钠与多巴胺治疗顽固性心衰的效果明显,不良反应较少,值得临床推广应用。展开更多
Certain amino acids changes in the human Na^(+)/K^(+)-ATPase pump,ATPase Na^(+)/K^(+)transporting subunit alpha 1(ATP1A1),cause Charcot-Marie-Tooth disease type 2(CMT2)disease and refractory seizures.To develop in viv...Certain amino acids changes in the human Na^(+)/K^(+)-ATPase pump,ATPase Na^(+)/K^(+)transporting subunit alpha 1(ATP1A1),cause Charcot-Marie-Tooth disease type 2(CMT2)disease and refractory seizures.To develop in vivo models to study the role of Na^(+)/K^(+)-ATPase in these diseases,we modified the Drosophila gene homolog,Atpα,to mimic the human ATP1A1 gene mutations that cause CMT2.Mutations located within the helical linker region of human ATP1A1(I592T,A597T,P600T,and D601F)were simultaneously introduced into endogenous Drosophila Atpαby CRISPR/Cas9-mediated genome editing,generating the Atpα^(TTTF)model.In addition,the same strategy was used to generate the corresponding single point mutations in flies(Atpα^(I571T),Atpα^(A576T),Atpα^(P579T),and Atpα^(D580F)).Moreover,a deletion mutation(Atpα^(mut))that causes premature termination of translation was generated as a positive control.Of these alleles,we found two that could be maintained as homozygotes(Atpα^(I571T)and Atpα^(P579T)).Three alleles(Atpα^(A576T),Atpα^(P579)and Atpα^(D580F))can form heterozygotes with the Atpαmut allele.We found that the Atpαallele carrying these CMT2-associated mutations showed differential phenotypes in Drosophila.Flies heterozygous for Atpα^(TTTF)mutations have motor performance defects,a reduced lifespan,seizures,and an abnormal neuronal morphology.These Drosophila models will provide a new platform for studying the function and regulation of the sodium-potassium pump.展开更多
文摘目的：观察微量泵持续注射硝普钠与多巴胺治疗顽固性心衰的临床疗效。方法：选择106例心功能Ⅲ-Ⅳ级顽固性心衰患者,采用微量泵持续泵入硝普钠和多巴胺进行顽固性心衰治疗,硝普钠起始剂量为6.25μg/min;同时采用另一微量泵持续泵入多巴胺,起始剂量为2 g/kg·min,直至血压下降至90-100 mm Hg;连续用药7 d,观察治疗后患者症状体征和心功能各参数的变化情况。结果：1106例顽固性心衰患者经硝普钠与多巴胺微泵治疗后,总有效率为85.85%（91/106）;2微量泵治疗后顽固性心衰患者的心率、血压、心胸比率、左室短轴缩短率、每搏输出量、每搏指数以及左室射血分数等参数较治疗前均有明显改善。结论：微量泵持续注射硝普钠与多巴胺治疗顽固性心衰的效果明显,不良反应较少,值得临床推广应用。
基金supported by the Natural Science Foundation of Fujian Province,No.2020J02027the National Natural Science Foundation of China,No.31970461the Foundation of NHC Key Laboratory of Technical Evaluation of Fertility Regulation for Non-human Primate,Fujian Maternity and Child Health Hospital,No.2022-NHP-05(all to WC).
文摘Certain amino acids changes in the human Na^(+)/K^(+)-ATPase pump,ATPase Na^(+)/K^(+)transporting subunit alpha 1(ATP1A1),cause Charcot-Marie-Tooth disease type 2(CMT2)disease and refractory seizures.To develop in vivo models to study the role of Na^(+)/K^(+)-ATPase in these diseases,we modified the Drosophila gene homolog,Atpα,to mimic the human ATP1A1 gene mutations that cause CMT2.Mutations located within the helical linker region of human ATP1A1(I592T,A597T,P600T,and D601F)were simultaneously introduced into endogenous Drosophila Atpαby CRISPR/Cas9-mediated genome editing,generating the Atpα^(TTTF)model.In addition,the same strategy was used to generate the corresponding single point mutations in flies(Atpα^(I571T),Atpα^(A576T),Atpα^(P579T),and Atpα^(D580F)).Moreover,a deletion mutation(Atpα^(mut))that causes premature termination of translation was generated as a positive control.Of these alleles,we found two that could be maintained as homozygotes(Atpα^(I571T)and Atpα^(P579T)).Three alleles(Atpα^(A576T),Atpα^(P579)and Atpα^(D580F))can form heterozygotes with the Atpαmut allele.We found that the Atpαallele carrying these CMT2-associated mutations showed differential phenotypes in Drosophila.Flies heterozygous for Atpα^(TTTF)mutations have motor performance defects,a reduced lifespan,seizures,and an abnormal neuronal morphology.These Drosophila models will provide a new platform for studying the function and regulation of the sodium-potassium pump.
