Abstract
Septic shock induces physiologic and hemodynamic responses that may alter the host's ability to metabolize an exogenous source of lipids. The present study examined the metabolic changes occuring during septic shock in the young animal receiving an intravenous fat emulsion. Five 8-wk-old male Beagle puppies were studied. Each animal served as his own control twice, during which time 14C-palmitic acid alone or with a 10% fat emulsion (Liposyn) was administered. Septic shock (cardiac output less than 50% of control) was induced with an intravenous bolus of live Escherichia coli. During shock the puppies received intravenous 14C-palmitic acid and Liposyn. The mean respiratory quotient for the shock dogs (0.96 ± 0.01) was significantly (p < 0.05) higher than that of the controls (0.83 ± 0.06). The amount of expired 14CO2 was 25.0 ± 15.9% for the shock animals, 53.9 ± 28.1% for the Liposyn controls, and 75.7 ± 30.5% for the controls receiving only 14C-palmitic acid (these differences are all significant, p < 0.05). After the onset of shock, serum triglyceride levels peaked within 2 min at 851 ± 540 mg/100 ml and remained elevated at 333 ± 213 mg/100 ml. Triglyceride levels in the Liposyn control animals returned to baseline values (54 ± 13 mg/100 ml) at the end of the 4-hr experimental period. Free fatty acids in the shock dogs reached a maximal level of 1.44 ± 0.09 mEq/liter at 1 hr and remained at this elevated value for a significantly longer period of time than in the Liposyn control puppies. Glycerol value followed a similar pattern and cholesterol remain unchanged. Plasma insulin in the shock animals steadily rose to a peak of 826 ± 358 μU/ml at the end of the experimental period; control animals showed no plasma insulin changes. The results of this study suggest that exogenous lipids administered during septic shock may not be metabolized as well as during the nonshock state. (Journal of Parenteral and Enteral Nutrition 8:652-656. 1984)
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