We conclude that endotoxin caused lung injury typical of ARDS as demonstrated by pulmonary edema, an increase in PaCO2, and a decrease in PaO2, a decrease in static lung compliance and inhibition of surfactant function. Exogenous surfactant treatment effected only moderate improvements in lung function (i.e., reduced venous admixture and restored surfactant function) in this sepsis-induced ARDS model.

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.

No abstract

No abstract