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.