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Departments of 1 Surgery, 2 Cell Biology and Physiology, 3 Pathology, 4 Medicine, and 5 Molecular Genetics and Biochemistry, and 6 University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15213
We tested the ability of a nitric oxide (NO)
scavenger to reduce tissue injury in a rodent model of hemorrhagic
shock. Rats were hemorrhaged to a mean arterial blood pressure (MAP) of
40 mmHg and then resuscitated when either 30% of their shed blood had
been returned (group 1) or after 100 min of
continuous shock (group 2). Selected animals
were treated with the NO scavenger NOX (30 mg · kg
1 · h1)
infused over 4 h. Hemorrhaged rats had a lower MAP after resuscitation compared with sham-shock control rats. NOX treatment significantly increased MAP after resuscitation from hemorrhage. Hemorrhagic shock
also increased liver injury as reflected by elevated ornithine carbamoyltransferase (OCT) plasma levels, and NOX treatment
significantly reduced OCT release. In addition, NOX was associated with
significantly decreased hepatic neutrophil infiltration and improved
24-h survival (n = 8 of 9) compared
with saline-treated shock animals (n = 3 of 9). These data suggest that excess NO mediates shock-induced tissue injury and that suppression of NO availability with NO scavengers may reduce the pathophysiological sequelae of severe hemorrhage.
nitric oxide synthase; trauma; kidney; multiple organ failure
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