Possible role of oxygen-derived, free radicals in cardiocirculatory shock.

The release of oxygen free radicals from ischemic myocardial tissue has been implicated as a causative factor of cell membrane damage and cardiac dysfunction in hemorrhagic shock. This study was done to determine whether or not hydrogen peroxide (H2O2) and superoxide ion (O2) are responsible for cardiac injury from hemorrhagic shock as indicated by reduced coronary perfusion and impaired contractile function. This hypothesis was tested by infusing selective O2 and H2O2 scavengers into anesthetized dogs in a state of shock, either during shock (group 3) or with fluid resuscitation (group 2) and comparing the cardiovascular response to that seen with shock and fluid resuscitation alone (group 1). We found no significant difference in shock induced derangements in myocardial oxygen metabolism or the degree of myocardial depression and regional ischemia in dogs in a state of shock given superoxide dismutase plus catalase, compared with shock alone. The results of our data suggested that, if O2 and H2O2 play a causative role in shock induced cardiac dysfunction or during reperfusion after shock, free radical scavengers must be administered early in the ischemic period. Furthermore, free radical scavengers administered with reperfusion do not enchance cardiac function nor myocardial perfusion.