Abstract 294: The Relationship Between Oxygen Administration and Oxidative Stress During Hemorrhagic Shock and Resuscitation
Objective: Hemorrhagic shock (HS) causes tissue hypoxia and following inflammation. Although supplemental oxygen is commonly administered in patients during HS, it has been considered that hyperoxia exacerbates inflammatory responses via oxidative stress. Thus, we hypothesized that oxygen administration during HS and fluid resuscitation contributes to oxidative stress.
Methods: Wistar male rats (224±15 g) were subjected to HS with and without supplemental oxygen administration (Oxy, n=5, N-Oxy, n=5). Controlled HS was induced by continuous withdrawing blood from left carotid artery for 60 min. Followed by shock period, shed blood (5.6±0.6 ml in N-Oxy, 5.1±0.8 ml in Oxy, P=0.35) and 10 ml of saline were infused for resuscitation up to 15 min. Systolic arterial pressure (FlucletTM), pH, PaO2, hemoglobin (iSTATTM), lactate (Lactate ProTM), derivatives of reactive oxygen metabolites (dROM), and biological antioxidant potential (BAP) (FreeTM) were assessed at baseline (C), the end of HS, and 60 min after resuscitation (R).
Results: Profiles of systolic arterial pressure and PaO2 at C, HS, and R were not differed between the groups (136±20 mmHg and 261±95 torr, 36±7 and 252±24, 96±19 and 294±59 in Oxy vs. 108±23 and 68±13, 38±10 and 98±23, 86±52 and 81±25 in N-Oxy, respectively, repeated ANOVA P=0.53 and P=0.22). DROMs decreased during HS in both groups (C to HS: 201±27 to 165±39 Carr Unit in Oxy vs. 233±39 to 204±41 in N-Oxy), whereas dROMs in Oxy increased on R (186±7) compared to N-Oxy (168±58, P=0.05). BAP had no differences between the two groups during the whole study period (C, HS, R: 2.6×103 ìM, 2.6×103, 2.6×103 in Oxy vs. 2.6×103, 3.6×103, 3.5×103 in N-Oxy, respectively, P=0.25). Oxidative stress (dROM/BAP) decreased during HS in both groups (C to HS: 0.08±0.01 to 0.06±0.01 in Oxy vs 0.09±0.01 to 0.07±0.00 in N-Oxy), but increased on R only in Oxy (0.07±0.00 vs 0.05±0.03 in N-Oxy, P=0.03). Profiles of arterial pH, lactate and hemoglobin had no differences between the groups.
Conclusions: Oxidative stress is suppressed during HS regardless of supplemental oxygen. However, oxygen administration exacerbates oxidative stress on post-hemorrhage resuscitation. These results suggest that hyperoxia may greatly contribute to oxidative stress during reperfusion.
- © 2010 by American Heart Association, Inc.