Role of fatty acids in the recovery of cardiac function during resuscitation from hemorrhagic shock

This study tested the hypothesis that removal of fatty acids as a fuel sour ce would improve cardiac efficiency at the expense of reduced cardiac contr actile function in the isolated working heart after hemorrhageretransfusion . Non-heparinized male Sprague-Dawley rats were anesthetized with ketamine- xylazine and were hemorrhaged to a mean arterial blood pressure of 40 mmHg for 1 h. Two-thirds volume of shed blood was reinfused together with 0.9% N aCl in a volume equal to 2.3 times the shed blood volume, followed by conti nuous infusion of 0.9% NaCl at 10 mL/kg per h for 3 h. Hearts were removed and perfused in closed, recirculating working mode for 60 min to measure hy draulic work and cardiac efficiency. Rates of glycolysis and glucose oxidat ion were assessed with [5-H-3/U-C-14] glucose (11 mM) in the absence or pre sence of 0.4 mM palmitate. Compared to baseline measurements, hemorrhageret ransfusion significantly reduced arterial blood glucose (228 +/- 7 versus 1 18 +/- 12 mg/dL) and non-esterified fatty acid concentrations (0.36 +/- 0.0 1 versus 0.30 +/- 0.02 mM), while elevating blood lactate (0.8 +/- 0.1 vers us 2.5 +/- 0.4 mM). Perfusion of sham hearts with glucose-only did not alte r cardiac work compared to shams perfused with glucose plus palmitate. Howe ver, shocked hearts perfused with glucose-only demonstrated a significant r eduction in cardiac work compared to shocked hearts perfused with glucose p lus palmitate and compared to sham hearts perfused with glucose only (P< 0. 05, repeated measures ANOVA). Shocked hearts perfused with glucose plus pal mitate showed no reduction in cardiac work compared to shams. Shocked heart s perfused with glucose-only had increased glucose oxidation rates compared to shams perfused with glucose plus palmitate. In sham hearts perfused wit h glucose-only, myocardial glycogen and triacylglycerol contents were signi ficantly reduced compared to hearts freeze-clamped in situ. These endogenou s fuels were not decreased in shocked hearts. These data indicate that hemo rrhagic shock renders the heart unable to mobilize endogenous fuels, and su ggest that withdrawal of fatty acid oxidation will impair myocardial energy metabolism during resuscitation.