title: Activating Na+-K+ ATPase: a potential cardioprotective therapy during early hemorrhagic shock.
abstract: Cell volume and resting potential are heavily affected by the activity of Na+-K+ ATPase (NKA, Na+-K+ pump), an essential membrane protein that regulates plasma K+ and Na+ levels. It is generally accepted that the ineffective perfusion of body tissues inhibits NKA activity and that NKA activity and heart failure are closely related. Recently, research has proven that the activation of NKA provides significant cardioprotection against ischemic injury. Based on these data, we propose that NKA stimulation could attenuate the development of heart arrhythmia during the early phase of hemorrhagic shock.
authors.affiliation: Beijing Institute of Transfusion Medicine, Beijing 100850, China.
authors.forename: Weijing
authors.initials: W
authors.lastname: Li
authors.affiliation: Beijing Institute of Transfusion Medicine, Beijing 100850, China.
authors.forename: Xuanlin
authors.initials: X
authors.lastname: Wang
authors.affiliation: Beijing Institute of Transfusion Medicine, Beijing 100850, China.
authors.forename: Min
authors.initials: M
authors.lastname: He
authors.affiliation: Beijing Institute of Transfusion Medicine, Beijing 100850, China.
authors.forename: Chunyan
authors.initials: C
authors.lastname: Wang
authors.affiliation: Beijing Institute of Transfusion Medicine, Beijing 100850, China.
authors.forename: Zhixin
authors.initials: Z
authors.lastname: Qiao
authors.affiliation: Shenzhou Biology & Technology Co., Ltd., Hohhot, Inner Mongolia 010206, China.
authors.forename: Qingjun
authors.initials: Q
authors.lastname: Wang
authors.affiliation: Beijing Institute of Transfusion Medicine, Beijing 100850, China. Electronic address: rensp12@yahoo.com.
authors.forename: Suping
authors.initials: S
authors.lastname: Ren
authors.affiliation: Beijing Institute of Transfusion Medicine, Beijing 100850, China. Electronic address: yuqun1970@gmail.com.
authors.forename: Qun
authors.initials: Q
authors.lastname: Yu
mesh_terms: D000200:Action Potentials; D000255:Adenosine Triphosphate / Q000737:chemistry; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000378:metabolism / Q000628:therapy; D002316:Cardiotonic Agents / Q000627:therapeutic use; D006321:Heart / Q000187:drug effects; D006801:Humans; D007511:Ischemia / Q000473:pathology; D008565:Membrane Proteins / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism; D051381:Rats; D012771:Shock, Hemorrhagic / Q000378:metabolism* / Q000628:therapy; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
chemical_list: D002316:Cardiotonic Agents; D008565:Membrane Proteins; D000255:Adenosine Triphosphate; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase