Abstract
Hypovolemic states are characterized by inadequate tissue perfusion; when this state is reversed, the reintroduction of oxygen is accompanied by the excess generation of oxyradicals and these, in turn, may cause “reperfusion injury” in susceptible tissues. When hemoglobin solution is used to resuscitate the hypovolemic state, the generation of oxyradicals may be enhanced by catalytic means. The generation of oxyradicals was estimated in dogs subjected to the acute removal of 35 ml/Kg blood, and resuscitated 45 mins thereafter with an equal volume of either autologous blood (Group I, n=6) or 6% stromafree hemoglobin solution (S.F.H.S.) (Group II, n=6). Hepatic and pancreatic enzymes were measured in blood drawn at intervals. The hypovolemic state was characterized by profound hypotension which was reversed by resuscitation. Oxyradical generation in arterial blood samples, drawn at various times, was estimated by the generation of oxidation products (2,3- and 2,5-dihydroxybenzoic acid) of exogenously administered sodium salicylate, determined by HPLC in plasma samples extracted with diethyl ether. Salicylate oxidation products rose significantly above the baseline value in Group I dogs, whereas they rose 5-6-fold higher than the baseline values in those of Group II. The actual values attained and the increments were significantly (p<05) greater in Group II than in Group I. In the group resuscitated with S.F.H.S., catalytically active iron concentration in plasma also rose 10-12-fold higher and was associated with spuriously elevated levels of gamma-glutamyl transferase due to interference with the assay. These findings are consistent with the hypothesis that blood-resuscitation of hypovolemic shock is accompanied by oxyradical generation of a modest degree; in contrast, S.F.H.S.-resuscitation introduces catalytically active iron and is accompanied by oxyradical generation of a significantly greater degree.