Superoxide Dismutase (SOD) Prevents Hypotension After Hemorrhagic Shock and Aortic Cross Clamping

Abstract

To determine if superoxide dismutase (SOD) administration attenuates injury caused by supraceliac aortic cross clamping, a randomized controlled study on 12 taconic rats was performed at the university hospital research center at Syracuse, New York. All animals were anesthetized and placed on a ventilator through a tracheotomy. Surgical preparation included catheterization of carotid and femoral arteries, and the jugular vein. A midline laparotomy was performed through which the supraceliac aorta was exposed and isolated. Animals were allowed to stabilize after surgery and baseline measurements [systemic pressure (Psys), central venous pressure, and blood gases] were recorded. Then, animals were subjected to 60 minutes of hemorrhagic shock (mean Psys = 35 mm Hg), followed by 45 minutes of supraceliac aortic cross clamping. After the release of the aortic cross clamp, shed blood was reinfused. After stabilization, all animals were monitored for 60 minutes. Rats were separated into two groups: the experimental group (n = 6) that received intravenous SOD before and during aortic cross clamping, and the control group (n = 6) that received an equivalent volume of saline at the same time periods. No difference was detected in overall arterial pH, partial arterial carbon dioxide pressure, or base excess at any time period between the groups. A significant increase in Psys was measured in the experimental group compared with the control group from the time of aortic cross-clamp release until the experiment was terminated. One hour after aortic cross-clamp release, the Psys for the experimental group was 69.2 +/- 10.6 mm Hg vs. 36.7 +/- 3.8 mm Hg for the control group (P < 0.05). These data demonstrate that superoxide dismutase significantly improves postaortic cross-clamp Psys. This suggests that oxygen-derived free radicals play a role in postaortic cross-clamp hypotension.

Extracellular Superoxide Dismutase Attenuates Lung Injury after Hemorrhage

“…Although previous studies have demonstrated the importance of superoxide in reperfusion injury (7)(8)(9)(10)(11)34), this is the first study to show that EC-SOD can attenuate hemorrhage-induced lung injury and suggests that the alveolar interstitial space and ECM play a role in superoxide-mediated lung injury. Our data suggest that elevated alveolar interstitial SOD activity may decrease the likelihood of developing acute inflammatory lung injury after hemorrhage.…”

“…For instance, hemorrhage-induced superoxide has recently been found to play a role in both the intracellular space and on the endothelial surface (7), and exogenously administered SOD, which sticks to endothelium, can ameliorate a hemorrhage-induced decrease in blood pressure (8) and survival (9)(10)(11). However, the role of ROS in the ECM of the alveolar interstitium, particularly for superoxide, has not been fully elucidated.…”

Monocyte Deactivation Correlates With Injury Severity Score, But Not With Heme Oxygenase-1 Levels in Trauma Patients

“…HO-1 and its three metabolites, carbon monoxide, biliverdin and free iron are known to possess anti-inflammatory properties (16). Several studies have suggested that HO-1 may limit tissue damage in response to different pro-inflammatory stimuli (17,18), and recent studies have shown that HO-1 mediates at least some of the anti-inflammatory effects of IL-10 (19,20). HO-1 can be induced under a variety of circumstances, including free radical stress, bacterial LPS exposure and hyperoxia, underscoring its importance as an immune mediator (16).…”

Effects of inhibitors of the activity of poly (ADP‐ribose) synthetase on the organ injury and dysfunction caused by haemorrhagic shock

“…The overproduction of ROS in haemorrhagic shock leads to a considerable oxidant stress as indicated by lipid peroxidation (Fleckenstein et al ., 1991; Hamano et al ., 1993) as well as the consumption of the endogenous antioxidant, vitamin E (Fleckenstein et al ., 1991). Interventions which reduce the generation or the effects of ROS exert beneficial effects in a variety of models of haemorrhagic shock (Allan et al ., 1986; Sanan et al ., 1989; Mannion et al ., 1994; Daughters et al ., 1996; Simon et al ., 1996; Fan et al ., 1998; Mota‐Filipe et al ., 1999).…”