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10.3892/etm.2017.4437 http://scihub22266oqcxt.onion/10.3892/etm.2017.4437 C5450562!5450562!28587398     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Exp+Ther+Med 2017 ; 13 (6): 3257-66 Nephropedia Template TP {{tp|p=28587398|t=2017. Diazoxide protects rat vascular endothelial cells against hypoxia and cold-induced damage |pdf=|usr=}}{{28587398}} gab.com Text Diazoxide protects rat vascular endothelial cells against hypoxia and cold-induced damage JO: Exp Ther Med http://www.kidney.de/pget.php?&tw=1&pmid=28587398 #FOAvip The present study aimed to examine the effects of hypoxia and cold on vascular endothelial cells (VECs), as well as the protective ability of novel VECs-protective drugs against these injuries. A rat model simulating exposure to hypoxia and cold at high altitude environments was established. Based on these animal experiments, rat aortic VECs were established as injury models and exposed to hypoxia and/or adrenaline (ADR) in vitro. The results revealed that hypoxia significantly altered the levels of nitric oxide and vascular endothelial growth factor, while the cold temperature significantly increased the release of ADR and noradrenaline. Exposure to hypoxia combined with cold temperature significantly affected all these indices. In vitro experiments demonstrated that hypoxia, ADR (which was used to simulate cold in the animal experiments) and the combination of the two factors resulted in damage to the VECs and endothelial dysfunction. In addition, the results also showed that diazoxide, a highly selective mitoKATP opener, protected VECs against these injuries. In conclusion, hypoxia and cold temperature induced endothelial cell dysfunction and endocrine disorders, respectively. Improving endothelial function using diazoxide may be an effective therapeutic strategy in patients with altitude-associated disorders. However, the potential for clinical application requires further study. Twit Text FOAVip Diazoxide protects rat vascular endothelial cells against hypoxia and cold-induced damage ????Exp Ther Med http://www.kidney.de/pget.php?&tw=1&pmid=28587398 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28587398 #FOAvip English Wikipedia <ref>{{Cite pmid|28587398}}</ref> Diazoxide protects rat vascular endothelial cells against hypoxia and cold-induced damage #MMPMID28587398 Zhang LC; Huang Z; Li PB; Nie HJ; Deng BN; Duan RF; Xiao ZH; Peng H; Feng H; Liu W Exp Ther Med 2017[Jun]; 13 (6): 3257-66 PMID28587398show ga The present study aimed to examine the effects of hypoxia and cold on vascular endothelial cells (VECs), as well as the protective ability of novel VECs-protective drugs against these injuries. A rat model simulating exposure to hypoxia and cold at high altitude environments was established. Based on these animal experiments, rat aortic VECs were established as injury models and exposed to hypoxia and/or adrenaline (ADR) in vitro. The results revealed that hypoxia significantly altered the levels of nitric oxide and vascular endothelial growth factor, while the cold temperature significantly increased the release of ADR and noradrenaline. Exposure to hypoxia combined with cold temperature significantly affected all these indices. In vitro experiments demonstrated that hypoxia, ADR (which was used to simulate cold in the animal experiments) and the combination of the two factors resulted in damage to the VECs and endothelial dysfunction. In addition, the results also showed that diazoxide, a highly selective mitoKATP opener, protected VECs against these injuries. In conclusion, hypoxia and cold temperature induced endothelial cell dysfunction and endocrine disorders, respectively. Improving endothelial function using diazoxide may be an effective therapeutic strategy in patients with altitude-associated disorders. However, the potential for clinical application requires further study. äDiazoxide protects rat vascular endothelial cells against hypoxia and (epmc).pdf DeepDyve Pubget Overpricing