Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
free free
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll Hepatocellular protection by nitric oxide or nitrite in ischemia and reperfusion injury Abe Y; Hines I; Zibari G; Grisham MBArch Biochem Biophys 2009[Apr]; 484 (2): 232-7Ischemia and reperfusion (I/R)-induced liver injury occurs in several pathophysiological disorders including hemorrhagic shock and burn as well as resectional and transplantation surgery. One of the earliest events associated with reperfusion of ischemic liver is endothelial dysfunction characterized by the decreased production of endothelial cell-derived nitric oxide (NO). This rapid post-ischemic decrease in NO bioavailability appears to be due to decreased synthesis of NO, enhanced inactivation of NO by the overproduction of superoxide or both. This review presents the most current evidence supporting the concept that decreased bioavailability of NO concomitant with enhanced production of reactive oxygen species initiates hepatocellular injury and that endogenous NO or exogenous NO produced from nitrite play important roles in limiting post-ischemic tissue injury.|*Liver Circulation[MESH]|Animals[MESH]|Cytokines/physiology[MESH]|Hepatocytes/drug effects/*physiology[MESH]|Humans[MESH]|Ischemia/*prevention & control[MESH]|Liver Transplantation/pathology/physiology[MESH]|Nitric Oxide/*pharmacology[MESH]|Nitrites/*pharmacology[MESH]|Reactive Oxygen Species/metabolism[MESH]|Reperfusion Injury/*prevention & control[MESH] |