Acute Hemorrhage and Oxygen Free Radicals

Prasad, Kailash; Kalra, Jawahar; Buchko, Greg
December 1988
Angiology;Dec1988, Vol. 39 Issue 12, p1005
Academic Journal
Oxygen free radicals are known to produce cellular injury. There are various mechanisms during hemorrhagic shock that can lead to an increase in the oxygen free radicals, which would produce a loss of membrane integrity and a decrease in cardiac function and cardiac contractility. The authors studied the effect of acute hemorrhage and reperfusion on the hemodynamics, blood lactate, and oxygen free radicals. Dogs were divided into two groups, group I, hemorrhagic shock and reinfusion; group II, hemorrhagic shock and reinfusion with superoxide dismutase (SOD) and catalase treatment. The dogs were bled (50% of the estimated blood volume) over a period of five to twelve minutes. After an hour of bleeding, the shed blood was transfused over twenty to twenty-five minutes. Group II received SOD (0.7 mg/kg, IV) and catalase (0.7 mg/kg, IV) within ten minues of bleeding. The hemodynamic measurements and collection of blood samples for measurement of oxygen free radicals and lactate were made before hemorrhage and at fifteen, thirty, and sixty minutes of hemorrhage and at fifteen, thirty, and sixty minutes after reperfusion of shed blood. There was a decrease in the cardiac function and index of myocardial contractility associated with an increase in the blood lactate after hemorrhage in group I. Similar but less marked changes in these parameters were observed in group 11. Recovery of hemodynamic parameters with reinfusion was better in group II as compared with that in group I. There was an increase in blood oxygen free radicals (superoxide anions) in group I, especially after reinfusion. No such changes were observed in group II. These results suggest that oxygen free radicals might be involved in acute hemorrhagic shock. Use of scavengers of oxygen free radicals might, therefore, be helpful in hemorrhagic shock.


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