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Department of Anesthesiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814
Previous studies
have shown that the liver is the first organ to display signs of injury
during hemorrhagic shock. We examined the mechanism by which pyruvate
can prevent liver damage during hemorrhagic shock in swine anesthetized
with halothane. Thirty minutes after the induction of a 240-min
controlled arterial hemorrhage targeted at 40 mmHg, hypertonic sodium
pyruvate (0.5 g · kg
1 · h1)
was infused to achieve an arterial concentration of 5 mM. The volume
and osmolality effects of pyruvate were matched with 10% saline (HTS)
and 0.9% saline (NS). Although the peak hemorrhage volume increased
significantly in both the pyruvate and HTS group, only the pyruvate
treatment was effective in delaying cardiovascular decompensation. In
addition, pyruvate effectively maintained the NADH/NAD redox state, as
evidenced by increased microdialysate pyruvate levels and a
significantly lower lactate-to-pyruvate ratio. Pyruvate also
prevented the loss of intracellular antioxidants (GSH) and a
reduction in the GSH-to-GSSG ratio. These beneficial effects on
the redox environment decreased hepatic cellular death by
apoptosis. Pyruvate significantly increased the ratio of Bcl-Xl (antiapoptotic molecule)/Bax (proapoptotic molecule), prevented the release of cytochrome c from mitochondria, and decreased
the fragmentation of caspase 3 and poly(ADP ribose) polymerase (DNA repair enzyme). These beneficial findings indicate that pyruvate infused 30 min after the onset of severe hemorrhagic shock is effective
in maintaining the redox environment, preventing the loss of the key
antioxidant GSH, and decreasing early apoptosis indicators.
glutathione; redox state; caspases
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