To determine whether muscular contractions obtained by electrical stimulation in immobilized patients are able to reduce muscle catabolism, we studied 10 patients (65-79 yr old) hospitalized in the intensive care unit for postoperative ventilatory failure or cerebral infarction. Artificial nutrition was the same for each patient during the 9-day study period. Two periods of 4 days were defined and randomized for each patient, separated by one day. During the muscular stimulation (MS) period, intermittent electrical stimulation of the muscles of the legs (external electrodes), were performed daily during 2 X 30 mn. During the other period, muscular stimulations were not performed. Urinary excretion of nitrogen (micro-Kjeldhal digestion and Nessler procedure), creatinine (Jaffe reaction), and 3-methyl histidine (3-MH) (gas phase chromatography) was measured every day. (table; see text) We conclude that a significant decrease in 3-MH and creatinine excretion is observed during the MS period. In intensive care unit patients, muscle protein breakdown may be influenced by intermittent muscular electrical stimulation.

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Effects of L-carnitine infusion on intralipid clearance and utilization. Study carried out in septic patients of an intensive care unit.

Endogenous and exogenous supplies of carnitine are decreased in septic patients under total parenteral nutrition, while carnitine urinary elimination is increased. But the increase of lipid role in the energetic cover requires a greater intervening role of tissue carnitine. So one may hope that in septic patients additional supply of L-carnitine would increase the catabolism of infused lipids. Twenty-eight septic patients, admitted in an intensive care unit were given parenteral nutrition (200 g of glucose, 12.5 g of N/24 hr). On the day of the study, 250 ml of Intralipid 20% (Kabi Vitrum) were administered in 4 hr. During the same period 13 patients were infused with 2 g of L-carnitine (Sigma-Tau). The remaining 15 patients constituted the control group. Basic plasma levels of triglycerides, nonesterified fatty acids, free glycerol, phospholipids, and ketone bodies remained within physiological limits. They increased during the lipid infusion and returned to initial values, 4 hr after the end of the infusion. Free and total carnitine levels and free/total carnitine ratio were comparable to healthy subjects' reference values. These parameters increased during L-carnitine infusion. This infusion had no effect on exogenous lipid clearance. However, it seemed to increase the uptake and the hepatic oxidation of circulating fatty acids. It invalidated the increase of lactate and pyruvate that had been noticed when lipids were solely infused.

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PubMedDate not supplied

Is vitamin K1 supplementation necessary in long-term parenteral nutrition?

BACKGROUND: I.v. lipid emulsions contain vitamin K in substantial quantities and in 1989, we therfore stopped supplying vitamin K1 to patients receiving home parenteral nutrition (HPN). METHODS: Nine patients (group I) receiving HPN before 1989 (10 mg i.v. vitamin K1 supplementation weekly until 1989, which was discontinued thereafter) and six patients with an initial low plasma vitamin K1 concentration (related to their malabsorption) (group II) receiving HPN after 1989 were studied. Prothrombin time (PT), plasma vitamin K1 concentration, and vitamin K1, content in lipid emulsions were measured throughout the period of HPN. RESULTS: All lipid emulsions, except for Eurolip 20% and Clinoleic 20% (Baxter SA, Maurepas, France) contained vitamin K1, with concentration ranges from 179 +/- 39 to 353 +/- 78 ng/L. Group I patients had an initial high plasma vitamin K1 concentration due to the vitamin K1 supplementation. After this supplementation was discontinued, plasma vitamin K1 decreased and remained in normal ranges with a normal PT. Throughout the HPN period after 1989, patients received 255 +/- 104 micrograms of vitamin K1 weekly through lipid emulsions. The PT and plasma vitamin K1 concentrations in group II patients were restored by lipid emulsions, which contained 418 +/- 143 micrograms/wk of vitamin K1. CONCLUSIONS: In patients receiving i.v. lipids (except for Eurolip and Clinoleic), a normal vitamin K1 status can be maintained during long-term HPN without vitamin K1 supplementation. However, vitamin K supplementation cannot be abandoned until the vitamin K content of emulsions is standardized by manufacturers. A weekly supply of 250 to 400 micrograms of vitamin K1 is enough to maintain and even restore a normal vitamin K1 status in HPN.

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