Time-Dependent Production of Endothelium-Related Biomarkers is Affected Differently in Hemorrhagic and Septic Shocks
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ORIGINAL ARTICLE
Time-Dependent Production of Endothelium-Related Biomarkers is Affected Differently in Hemorrhagic and Septic Shocks Cenk Nuri Coskun,1,4 Suzan Emel Usanmaz,2 Vahide Savci,3 and Emine Demirel-Yilmaz2
Shock is associated with inflammation-induced endothelial dysfunction. The aim of this study was to determine time-dependent alteration of blood biomarkers related to endothelial function in hemorrhagic and septic shocks. Hemorrhagic shock was induced by bleeding the animals. A cecal ligation and incision model was used to induce septicemia. Resuscitation was carried out by infusion of lactated Ringer’s solution. Resuscitation extended survival time in both shock groups. Blood pressure increased by resuscitation in the hemorrhagic shock but not in the septic shock. While hemorrhage caused a decrease in plasma levels of nitric oxide (NO) and hydrogen sulfide (H2S), asymmetric dimethylarginine (ADMA) and total antioxidant capacity (TAC) levels were increased. Only NO and TAC levels at the late phase were reversed by resuscitation. On the other hand, plasma levels of NO, ADMA, and TAC were increased by septicemia and resuscitation did not alter the septicemia-induced increase. These results indicate that blood biomarkers related to endothelial function were differentially affected by hemorrhage and septicemia. The time scale of biomarker production should be taken into consideration for the diagnostic and therapeutic approaches to these lifethreatening diseases.
Abstract—
KEY WORDS: hemorrhagic shock; septic shocks; NO; ADMA; TAC; H2S.
INTRODUCTION Circulatory shock is an acute, life-threatening disease characterized by reduced effective blood flow of the body tissues. In addition, a systemic inflammatory response is also present during shock. Hemorrhage and 1
Faculty of Medicine, Department of Medical Pharmacology, Duzce University, Konuralp, 81620 Duzce, Turkey 2 Faculty of Medicine, Department of Medical Pharmacology, Ankara University, Sihhiye, 06100 Ankara, Turkey 3 Faculty of Medicine, Department of Medical Pharmacology, Uludag University, 16240 Bursa, Turkey 4 To whom correspondence should be addressed at Faculty of Medicine, Department of Medical Pharmacology, Duzce University, Konuralp, 81620 Duzce, Turkey. E-mail: [email protected]
sepsis are the most common causes of circulatory shock in humans [1, 2]. Functions of the endothelium in circulatory shock are critically important for vascular response and host survival. Although the exact mechanism of shock remains unknown, it has been suggested that endothelial dysfunction is probably the cause and/or result of the general inflammatory response [3, 4]. Systemic activation and dysfunction of the endothelium always end in inadequate tissue perfusion and blood-tissue barrier disruption. With increasing dysfunction, uncontrolled clotting activation, capillary microthrombi formation, tissue edema, local hypoxia, and ischemia are initiated. This in turn enhances a vicious cycle leading to multiple organ failure and death [5–7].
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