0.7 EFFECT OF L-CARNITINE AND FAT EMULSION IN ISOLATED PERFUSED PIG LIVER. St. v. Sommoggy, A. Lohninger*, R. Hickman**, J. Terblanche** (Chir. Klinik und Poliklinik der Technischen Universitat Miinchen, FRG;) (* I. Med.-Chem. Institut der Universitat Wien, Austria) (**Department of Surgery, University of Cape Town, RSA)

Optimal infusion therapy in liver cell damage is still an unsolved problem Damaged liver cells show a progressive' loss in phospholipids, which leads to an impairment of membranes of mitochondria and microsomes. By the re- sulting changes in membrane function cell damage becomes irreversible and leads ultimately to cell death. In this study effects of fat emulsion and L-Carnitine administration havebeen studied in the isolated perfused liver circuit.Perfusion timer 4 hours, each group n=5. Fat emulsion showed a mar- ked decrease in portal venous flow (652+63,4 to 254+147,8 ml/min), which was not influenced by L-Carnitine administration. Hepatic artery flow in the fat emulsion group showed a slight decrease (55,8+12,3 to 51,6+9,9 ml/min), which was markedly enhanced by the additional L-Carnitine admi- nistration (83,8218,5 to 56,8~17,0 ml/min). A marked increase in FFA- levels in the fat emulsion group (0,44~0,25 to 0,612 34 bmol/l) could be completely suppressed by the additional L-Carnitine administration (0,23+0,14 to 0,24~0,1 bmol/l). An increase of phospholipid degradation products could be shown by means of thin layer chromatography and gas- liquid chromatography. Characterisation of these degradation products was performed by mass spectrometry. Carnitine provides by utilization of FFA more energy substrate to the li- ver cells, increases perfusion and prevents accumulation of acyl-coenzyme A esters of long chain fatty acids which inhibite several mitochondrial enzymes, Acyl-coenzyme A esters are transformed to the corresponding Car- nitine-esters and a general improvement of cell metabolism results.

0.8 EFFECTS OF CARNITINE SUPPLEMENTATION ON TISSUE CARNITINE LEVELS AND FATTY ACID OXIDATION IN WEANLING RATS GIVEN TOTAL PARENTERAL NUTRITION (TPN). H.C. Meng, T. Urushibara (Departments of Physiology and Surgery, Vanderbilt University, Nashville, TN, USA). We and others have observed a decrease in plasma carnitine in adults as well as in infants on TPN. The present work is to study the correlation of plasma, tis- sue and urine carnitine levels and fatty acid oxidation in vivo and in various tissues in vitro. Eighteen weanling male Sprague-Dawley rats were divided into three groups of 6 in each: 1. TPN + carnitine, 2. TPN - carnitine, 3. Rat chow fed orally ad lib. The TPN infusate contained amino acids, glucose, vitamins, electrolytes and inorganic trace minerals; about 22, 68 nd 1Oo/o calories was supplied by amino acids, glucose and fat (Intralipi , 1OO/o), respec- k tfvely. L-carnitine, 100 mg/lOO gm body weight, was added to TPN solution daily. Weight gain, caloric and nitrogen intake of orally fed rats were slightly greater than those maintained on TPN. Rats given TPN + carnitine showed a greater weight gain with less energy and nitrogen intake than those given no carnitine. Plasma carnitine was higher in rats on TPN + carnitine than that in rats fed orally; it was lower in rats given TPN - carnitine than that of orally fed animals. Similar pattern was observed for liver short-chain carnitine in these three groups of rats. The liver long-chain carnitine in rats on TPN + carnitine was lower than that of orally fed rats, but it was slightly higher than that of rats on TPN - carnitine. Weekly urinary carnftine levels were markedly elevated throughout in rats on TPN + carnitine but they

In vitro oxidation of rf re progressively decreased in those on TPN -

carnitine. C-l-palmitate was less in livers and skeletal muscles from rats on TPN - c rnitine than that from rats on TPN + carnitine. The-in ~vivo oxidation of &-I-palmi_tate was similar in both groups of TPN rats. It seems that TPN depletes body carnitine. Carnitine appears required for optimal fat utilization,

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