Interstitial Metabolic Monitoring During Hemorrhagic Shock
Final rept. 15 Mar 2004-14 Oct 2006
HENRY M JACKSON FOUNDATION FOR THE ADVANCEMENT OF MILITARY MEDICINE ROCKVILLE MD
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Decompensation in hemorrhagic shock is the critical stage after which resuscitative efforts may prove futile. We hypothesize that decompensation results from K-mediated vasodilation andor loss of cardiac contractility. Anesthetized rats were bled to a constant mean arterial pressure of 40 mmHg and subsequent resuscitated with normal saline at early pre-decompensatory and late decompensatory stages of shock. In the first set of experiments, microdialysis probes were implanted in skeletal muscle for continuous assessment of potassium and other metabolic markers. In a second set of experiments, animals underwent left heart catheterization and continuous measurement of cardiac contractility during hemorrhage and resuscitation. At the end of experiments, tissues were harvested for ex vivo Na,K-ATPase NKA activity. K concentrations in muscle interstitium were significantly higher in hemorrhaged animals than controls 2.34 times baseline vs. 1.24, p 0.05, this difference was not reflected in blood values. NKA in early and late hemorrhagic shock was increased vs. controls in skeletal and cardiac muscle. Cardiac contractility fell with hemorrhage but was restored with resuscitation in both early and late shock. These results suggest that decompensation results from a loss of peripheral rather than cardiac responsiveness.
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