• Jodie H Taylor, Greg J Beilman, Mark J Conroy, Kristine E Mulier, Dean Myers, Angelika Gruessner, and Bruce E Hammer.
• Department of Surgery, University of Minnesota, Minneapolis, Minnesota 55455, USA.
• Shock. 2004 Jan 1;21(1):58-64.

AbstractThe defect in energy production in an organism during shock states may be related to the impairment of mitochondrial respiration early in shock. The aim of this study was to investigate the timing and degree of cellular energetic changes during hemorrhagic shock in real time. Instrumented, splenectomized swine were randomized to undergo hemorrhagic shock, induced by a 35% blood volume bleed, for 90 min with (n = 10) or without (n = 9) subsequent resuscitation. Resuscitated animals received shed blood in two increments followed by two normal saline boluses (20 mL/kg/bolus). Throughout experimentation, tissue phosphoenergetics of liver and skeletal muscle were monitored using 31P nuclear magnetic resonance (NMR) spectroscopy via NMR coils on the liver and hindlimb. Near-infrared spectroscopy probes were used to measure liver, stomach, and skeletal muscle oxyhemoglobin saturation (StO2). Hemorrhagic shock induced an increase in phosphomonoesters in skeletal muscle (baseline: 7.09%, 90 min: 9.94% (P < 0.05); expressed as percent total phosphorus). This increase resolved in animals receiving resuscitation (n = 10) but remained elevated in those in unresuscitated shock (n = 9). Inorganic phosphate levels increased and betaATP levels decreased significantly in the liver of animals in shock as compared with baseline. StO2 in skeletal muscle, stomach, and liver correlated with whole organism oxygen delivery (r2 = 0.356, 0.368, and 0.432, respectively). We conclude that hemorrhagic shock induces early elevation of phosphomonoesters in skeletal muscle, which correlates with the severity of shock. This implies an early transition to anaerobic glycolysis during hemorrhagic shock, which may be indicative of early mitochondrial dysfunction.

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