Sepsis is related to hyper-inflammatory reactions inresponse to bacterial infections.1 The overwhelmingimmune responses that occur in sepsis, which are mediatedby various mediators of vascular inflammatory, lead toshock, multiple organ damage and even death.1 As shockprogresses, metabolic acidosis worsens and blood pHdecreases.2,3 Patients with sepsis experience lactic acidosiscaused by respiratory failure, shock and kidney failure, andincreased mortality due to a decrease in venous oxygensaturation.2,3 Additionally, under normal physiological con-ditions, the vascular endothelium plays central roles in theregulation andmaintenance of vascular integrity in responseto the extracellular environment, and therefore, it is theprimary target site of sepsis-induced damage.4 Because all