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  • Title: Beneficial effects of antioxidants in hemorrhagic shock.
    Author: Kapoor R, Prasad K.
    Journal: Angiology; 1995 Apr; 46(4):281-97. PubMed ID: 7726448.
    Abstract:
    The present study was undertaken to investigate the role of endogenous hydrogen peroxide (H2O2) in cardiac depression and cytotoxicity during hemorrhagic shock and reinfusion. To achieve this objective, the changes in the cardiac function and contractility, plasma creatine kinase (CK) and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL), and cardiac malondialdehyde (MDA) concentration in anesthetized dogs were determined before and during shock and reinfusion in the presence of absence of catalase (a metabolizer of H2O2). The dogs were divided into three groups randomly. Group I: sham, four hour duration; group II: two hours of shock followed by two hours of reinfusion; group III: same as group II but pretreated with catalase. Hemorrhage shock was produced in the dogs by lowering the mean arterial pressure to 50 +/- 5 mm Hg by bleeding into standard blood bank bags containing 63 mL of citrate, phosphate, dextrose, and adenine (CPDA) anticoagulant for 450 mL of blood. The shock was maintained for two hours by bleeding or reinfusing the shed blood as needed. Cardiac function and contractility were depressed while plasma CK, CK-MB, and lactate increased during shock. Reinfusion after two hours of shock tended to return hemodynamic parameters and plasma lactate levels toward control values. Plasma CK and CK-MB and PMNL-CL increased further. Cardiac MDA content also increased after shock and reinfusion, suggesting oxidative damage. Pretreatment with catalase attenuated the deleterious effects of shock and reinfusion on the cardiovascular function and contractility, and the rise in plasma CK, CK-MB, and lactate, PMNL-CL, and cardiac MDA. However, the protection with catalase was not complete. These results suggest that hydrogen peroxide (H2O2) may partly be involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.
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