0.47 EFFECTS OF INFUSING DIFFERENT RATES OF INTRALIPID IN VENTILATED PATIENTS. P.Sin er &ire B. Venus, S. Bursztein, D. Katz, V. Kvetan, J. Askanazi. Departments of Cri ica

Medicine, Rambam Medical Center, Haifa, Israel. Montefiore Medical Center, Bronx, NY, and Memorial Center Jacksonville, FL.

Changing the concentrationof infused arachidonic acid modifies pulmonary vascular resistance , possible due to proportions of Prostacyclin and Thromboxane metabolites. (6keto PGFla and TXB2). This study evaluated variations of hemodynamic and respiratory parameters and prostaglandin metabolites during slow and rapid infusion of intravenous fat emulsions (IVFE) in critically ill patients needing mechanical ventilatory support.

Eight patients received, in a random crossover fashion, 500ml of intralipid 20% over a period of 6 hours and 24 hours as part of their TPN regimen. Fat was given at 0.25 + 0.04 g/Kg/h and 0.06 + 0.01 g/Kg/h (mean&SD). Intrapulmonary shunt (Qs/Qt), mean pulmonary artery pressure (MPAP), cardiac output (CO), oxygen consumption (VO2) and delivery (902) were measured at 0,6 and 24 hours. Serum was assayed for 6kPGFla and TXB2 in 6 patients. After bolus infusion, a significant increase in CO, MPAP and Q02 were observed (p < 0.5, 0.001 and 0.02 respectively). At the end of the slow infusion rate, a significant decrease in V02 (p c 0.021, and increase in shunt (p < 0.02) and in 6kPGFla (P < 0.02) and in 6kPGFla (P < 0.05) were noted when compared to control.

These results confirm that rapid infusion of IVFE induces pulmonary vasoconstriction and decreases 02 utilization, while a slow infusion rate induces pulmonary vasodila- tion and an increase in prostacyclin metabolite. This vasodilation, with increased antiinflammatory prostaglandin metabolites, could be beneficial in acute respiratory failure.

0.48 ElTEClS OF GLUCOSE ON MAINOURISHED PATIENTS Gm HIGH N INTAKES. R.A.Forse, D.H.Elwyn J.Askanazi, J.M.Kinney. Departments of Surgery aad Anesthesiology, Colmbia Dniversity: New York, U.S.A.

Twelve malnourished patients were given 5% dextrose(D5W) for 2 days then randcanized to receive higblor each.InkJkg day

_$w glucose paxateral nutrition followed by the other for 8 days : protein intake was 59(500 nq N) and fat intake was 6 on both reg-

imens; gluco=_.ta&f was 30 on the low and 105 on the high glucose diet. N bal(ng kg day ) was I$39 9th D5R ‘; at zero energybalit was +47. Resting energy

expenditure(mE), 105 kJ kg day on D5W, increased(p(O.05) to 118 and 119 on the low and high diets. Results are cm to a previous(Clin Sci 72:489,1987) almost identic- Table 1. Differences betwaen high and al study with a lcw(155 mg/kg) daily N intake. low(H-L) glucose diets. Mean t SIX Increase inNbalwith increasing glucosewas

Iow N in High N in twice as high with the high N intake(Table 1). N bal/E bal(nq_w) 0.28+0.08 0.6OtO.25 added glucose increased RHE and cm&nine(C) ex- =S&Jkg ,day ,) llf2 lf3 C(nq N ki-'dam",

cretion on the low but not the high N intake. 0.8t0.2 O.lfO.l Glycog~ deposition during high glucose was 6.4

s/kg on the low N but onlv 1.4 on the hiuh N intake. Plasma insulin and ulucaaon were higher aud FFA lmax on high than on low-21 intake(Table 21.A significant'redu&ion in Table 2. Plasma concentrations(~). Mean t SEM. PcO.05 frceu D5W*. low?! alucaaon occur-

D5W -Itw glucose High glucose' i&w&h the LawN HighN UxiN HighN IowN High N high but not

Glucose 6.OkO.3 7.351.0 6.0fO.l 6.1f0.3 6.7+0.2*# 8.3f1.2# the low N diet. FFA IIlSUlitl

0.8",:",.09 0.::3",.05 0.69+0.10 0.42f0.04*0.59f0.07*0.29f0.03*# The metabolic 14t3 25+4* 27f7*# 48?4*# effects of sluc-

Glucagon 129+24 197f119 136f21 557fllO* 125f21 -- 398f68*# ose a&in&rat- ionappear tobeminlymadiatedS;r insulina~~Xi&~andbv &ii iilsuiinand glucagon at high N intakes. This &y help explain the differences & the effects of glucose loads on REE, glycogen deposition, and creatinine excretion between the 2 diets.

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