ROLE OF OXYRADICALS IN CARDIOVASCULAR DEPRESSION AND CELLULAR INJURY IN HEMORRHAGIC-SHOCK AND REINFUSION - EFFECT OF SOD AND CATALASE

We investigated the effects of hemorrhagic shock and reinfusion on the cardiac function and contractility, plasma CK and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonucl ear leukocytes (PMNL-CL), cardiac chemiluminescence (LV-CL), antioxida nt enzymatic activity [superoxide dismutase (SOD), catalase, glutathio ne peroxidase (GSH-P-X)], and malondialdehyde (MDA) concentration in a nesthetized dogs, to determine the role of oxyradicals in cardiac depr ession and cellular injury in hemorrhagic shock and reinfusion. The do gs were assigned to four groups: group I (sham), 4 hrs duration; group II, 4 hr of shock; group III, 2 hr of shock, followed by reinfusion f or 2 hr; and group IV, as in group III, but pretreated with SOD and ca talase. Hemorrhagic shock was produced by withdrawing blood to maintai n the mean arterial pressure at 50 +/- 5 mm Hg. Cardiac function and c ontractility were depressed during hemorrhagic shock. Plasma CK; CK-MB and lactate; and cardiac MDA, Mn-SOD, and CuZn-SOD increased, while c atalase activity decreased during shock. Following reinfusion after 2 hr of shock, hemodynamic parameters and plasma lactate tended to retur n toward control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total SOD, Mn- and CuZn-SOD increased further, while LV-CL and GSH-P, decreased. In spite of the increased antioxidant reserve, oxidative d amage was noted. Pretreatment with SOD and catalase attenuated the del eterious effects of shock and reinfusion on the cardiovascular functio n, plasma CK, CK-MB, and lactate, PMNL-CL, cardiac MDA and SOD, and LV -CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals (O-2(-), H2O2) ma y be partly involved in the deterioration of cardiovascular function a nd cellular injury during hemorrhagic shock and reinfusion. (C) 1994 W iley-Liss, Inc.