Operating room management: why, how and by whom?

Operating room (OR) is a cost-intensive environment, and it should be managed efficiently. When improving efficiency, shortening case duration by parallel processing, training of the resident surgeons, the choice of anesthetic methods, effective scheduling, and monitoring of the overall OR performance are important. When redesigning the OR processes, changes should be given a clear target and the achieved results monitored and reported to everyone involved. Advanced, reliable, and easy to use information technology solutions for OR management are under development. Pre-operative clinic and functionally designed facilities support efficiency. OR personnel must be kept motivated by clear management and leadership, supported by superiors.

Insulin resistance of glucose uptake in skeletal muscle cannot be ameliorated by enhancing endothelium-dependent blood flow in obesity.

We tested the hypothesis that endothelium-dependent vasodilatation is a determinant of insulin resistance of skeletal muscle glucose uptake in human obesity. Eight obese (age 26+/-1 yr, body mass index 37+/-1 kg/m2) and seven nonobese males (25+/-2 yr, 23+/-1 kg/m2) received an infusion of bradykinin into the femoral artery of one leg under intravenously maintained normoglycemic hyperinsulinemic conditions. Blood flow was measured simultaneously in the bradykinin and insulin- and the insulin-infused leg before and during hyperinsulinemia using [15O]-labeled water ([15O]H2O) and positron emission tomography (PET). Glucose uptake was quantitated immediately thereafter in both legs using [18F]- fluoro-deoxy-glucose ([18F]FDG) and PET. Whole body insulin-stimulated glucose uptake was lower in the obese (507+/-47 mumol/m2 . min) than the nonobese (1205+/-97 micromol/m2 . min, P < 0.001) subjects. Muscle glucose uptake in the insulin-infused leg was 66% lower in the obese (19+/-4 micromol/kg muscle . min) than in the nonobese (56+/-9 micromol/kg muscle . min, P < 0.005) subjects. Bradykinin increased blood flow during hyperinsulinemia in the obese subjects by 75% from 16+/-1 to 28+/-4 ml/kg muscle . min (P < 0.05), and in the normal subjects by 65% from 23+/-3 to 38+/-9 ml/kg muscle . min (P < 0.05). However, this flow increase required twice as much bradykinin in the obese (51+/-3 microg over 100 min) than in the normal (25+/-1 mug, P < 0.001) subjects. In the obese subjects, blood flow in the bradykinin and insulin-infused leg (28+/-4 ml/kg muscle . min) was comparable to that in the insulin-infused leg in the normal subjects during hyperinsulinemia (24+/-5 ml/kg muscle . min). Despite this, insulin-stimulated glucose uptake remained unchanged in the bradykinin and insulin-infused leg (18+/-4 mumol/kg . min) compared with the insulin-infused leg (19+/-4 micromol/kg muscle . min) in the obese subjects. Insulin-stimulated glucose uptake also was unaffected by bradykinin in the normal subjects (58+/-10 vs. 56+/-9 micromol/kg . min, bradykinin and insulin versus insulin leg). These data demonstrate that obesity is characterized by two distinct defects in skeletal muscle: insulin resistance of cellular glucose extraction and impaired endothelium-dependent vasodilatation. Since a 75% increase in blood flow does not alter glucose uptake, insulin resistance in obesity cannot be overcome by normalizing muscle blood flow.

Role of blood flow in regulating insulin-stimulated glucose uptake in humans. Studies using bradykinin, [15O]water, and [18F]fluoro-deoxy-glucose and positron emission tomography.

Defects in insulin stimulation of blood flow have been used suggested to contribute to insulin resistance. To directly test whether glucose uptake can be altered by changing blood flow, we infused bradykinin (27 microgram over 100 min), an endothelium-dependent vasodilator, into the femoral artery of 12 normal subjects (age 25+/-1 yr, body mass index 22+/-1 kg/m2) after an overnight fast (n = 5) and during normoglycemic hyperinsulinemic (n = 7) conditions (serum insulin 465+/-11 pmol/liter, 0-100 min). Blood flow was measured simultaneously in both femoral regions using [15O]-labeled water ([15O]H2O) and positron emission tomography (PET), before and during (50 min) the bradykinin infusion. Glucose uptake was measured immediately after the blood flow measurement simultaneously in both femoral regions using [18F]-fluoro-deoxy-glucose ([18F]FDG) and PET. During hyperinsulinemia, muscle blood flow was 58% higher in the bradykinin-infused (38+/-9 ml/kg muscle x min) than in the control leg (24+/-5, P<0.01). Femoral muscle glucose uptake was identical in both legs (60.6+/-9.5 vs. 58.7+/-9.0 micromol/kg x min, bradykinin-infused vs control leg, NS). Glucose extraction by skeletal muscle was 44% higher in the control (2.6+/-0.2 mmol/liter) than the bradykinin-infused leg (1.8+/-0.2 mmol/liter, P<0.01). When bradykinin was infused in the basal state, flow was 98% higher in the bradykinin-infused (58+/-12 ml/kg muscle x min) than the control leg (28+/-6 ml/kg muscle x min, P<0.01) but rates of muscle glucose uptake were identical in both legs (10.1+/-0.9 vs. 10.6+/-0.8 micromol/kg x min). We conclude that bradykinin increases skeletal muscle blood flow but not muscle glucose uptake in vivo. These data provide direct evidence against the hypothesis that blood flow is an independent regulator of insulin-stimulated glucose uptake in humans.

Intact insulin stimulation of skeletal muscle blood flow, its heterogeneity and redistribution, but not of glucose uptake in non-insulin-dependent diabetes mellitus.

We tested the hypothesis that defects in insulin stimulation of skeletal muscle blood flow, flow dispersion, and coupling between flow and glucose uptake contribute to insulin resistance of glucose uptake in non-insulin-dependent diabetes mellitus (NIDDM). We used positron emission tomography combined with [15O]H2O and [18F]-2-deoxy--glucose and a Bayesian iterative reconstruction algorithm to quantitate mean muscle blood flow, flow heterogeneity, and their relationship to glucose uptake under normoglycemic hyperinsulinemic conditions in 10 men with NIDDM (HbA1c 8.1+/-0.5%, age 43+/-2 yr, BMI 27.3+/-0.7 kg/m2) and in 7 matched normal men. In patients with NIDDM, rates of whole body (35+/-3 vs. 44+/-3 micromol/kg body weight.min, P < 0.05) and femoral muscle (71+/-6 vs. 96+/-7 micromol/kg muscle.min, P < 0.02) glucose uptake were significantly decreased. Insulin increased mean muscle blood flow similarly in both groups, from 1.9+/-0.3 to 2.8+/-0.4 ml/100 g muscle.min in the patients with NIDDM, P < 0.01, and from 2.3+/-0.3 to 3.0+/-0.3 ml/100 g muscle.min in the normal subjects, P < 0.02. Pixel-by-pixel analysis of flow images revealed marked spatial heterogeneity of blood flow. In both groups, insulin increased absolute but not relative dispersion of flow, and insulin-stimulated but not basal blood flow colocalized with glucose uptake. These data provide the first evidence for physiological flow heterogeneity in human skeletal muscle, and demonstrate that insulin increases absolute but not relative dispersion of flow. Furthermore, insulin redirects flow to areas where it stimulates glucose uptake. In patients with NIDDM, these novel actions of insulin are intact, implying that muscle insulin resistance can be attributed to impaired cellular glucose uptake.

Effects of insulin on blood flow and volume in skeletal muscle of patients with IDDM: studies using [15O]H2O, [15O]CO, and positron emission tomography.

Exaggerated vasoconstriction and blunted vasodilation of peripheral resistance arteries to various vasoactive agents characterize patients with IDDM. We characterized the hemodynamic effects of insulin in skeletal muscle in patients with IDDM. Muscle blood flow and blood volume were measured basally and during a high-dose insulin infusion (5 mU x kg(-1) x min[-1]) in seven normotensive patients with IDDM (age, 30 +/- 6 years; BMI, 24.5 +/- 2.0 kg/m2; blood pressure, 124 +/- 12/78 +/- 11 mmHg) and nine matched normal subjects, using [15O]H2O, [15O]CO, and positron emission tomography (PET). Whole-body insulin sensitivity was determined using the euglycemic insulin clamp technique. Insulin-stimulated whole-body glucose uptake was significantly lower in the patients with IDDM (45 +/- 15 micromol x kg(-1) x min[-1]) than in the normal subjects (62 +/- 14 micromol x kg(-1) x min[-1]) (P < 0.05). Insulin increased muscle blood flow by 111 +/- 69% above basal from 3.0 +/- 2.0 to 5.8 +/- 3.0 ml x 100 g(-1) muscle x min(-1) (P < 0.005) in the normal subjects, but only by 42 +/- 30% from 2.0 +/- 0.9 to 2.9 +/- 1.4 ml x 100 g(-1) muscle x min(-1) (P < 0.005) in patients with IDDM (P < 0.05 for change in flow in IDDM vs. normal subjects). The calculated muscle vascular resistances were comparable basally, but higher during hyperinsulinemia in the patients with IDDM (37 +/- 17 mmHg x 100 g x min x ml[-1]) than in the normal subjects (16 +/- 7 mmHg x 100 g x min x ml[-l]) (P < 0.05). Muscle blood volume increased significantly by insulin in both groups without any difference between the groups. We conclude that the ability of supraphysiological concentrations of insulin to stimulate muscle blood flow is blunted in patients with IDDM, because of the inability of insulin to stimulate linear flow velocity rather than blood volume in skeletal muscle. This defect adds yet another defect to the list of abnormalities in vascular function in IDDM, which might predispose these patients to develop hypertension.

Successful treatment of whiplash-type injury induced severe pain syndrome with epidural stimulation: a case report.

Chronic severe cervico-facial pain syndrome associated with a whiplash-type injury was successfully treated with epidural spinal cord stimulation. The patient had been in pain for 9 years, responding temporarily only to stellate ganglion blocks. The patient has now been painless for 18 months. We have been unable to find a similar case reported in the literature to date.

Insulin resistance in essential hypertension is characterized by impaired insulin stimulation of blood flow in skeletal muscle.

OBJECTIVE: To determine whether insulin-stimulated blood flow in patients with mild essential hypertension is altered. SUBJECTS: Eleven untreated mildly hypertensive patients [aged 35 +/- 2 years, body mass index 25.1 +/- 0.4 kg/m2, mean arterial pressure 110 +/- 2 mmHg (means +/- SEM) and 10 matched normotensive subjects (mean arterial pressure 94 +/- 3 mmHg). METHODS: Blood flow was quantitated directly in skeletal muscle both basally and during supraphysiologic hyperinsulinemia (serum insulin approximately = 450 mU/l) using radiowater ([15O]H2O) and positron emission tomography. Whole-body and femoral muscle glucose uptakes were determined using the euglycemic insulin clamp technique, [18F]-2-fluoro-2-deoxy-D-glucose and positron emission tomography. RESULTS: Rates of whole-body and femoral muscle glucose uptake were significantly lower in the hypertensive than in the normotensive group. Insulin increased muscle blood flow by 91% in the normotensive group, but only by 33% in the hypertensive group. CONCLUSIONS: The ability of insulin to stimulate blood flow in patients with mild essential hypertension is impaired.

Transport of carbon-11-methionine is enhanced by insulin.

UNLABELLED: The anabolic effects of insulin are not restricted to carbohydrate and lipid metabolism but also include protein metabolism. However, the effects of insulin on protein metabolism have been difficult to demonstrate in vivo. Amino acid transport is partly regulated by insulin according to the experimental data. PET provides a way to measure fractional uptake rates of amino acids. The purpose of this study was to measure the effect of insulin on amino acid transport from the plasma to the human parotid glands. METHODS: We compared the uptake of L-[methyl-11C]methionine ([11C]methionine) into the parotid glands and cerebellum in seven healthy volunteers during the fasting state and euglycemic insulin clamp technique (1 mU/kg per minute). RESULTS: The fractional uptake rate of [11C]methionine was increased by 31% for the right parotid gland (p = 0.003) and by 29% for the left parotid gland (p = 0.009) during insulin clamp, while the increase was 19% for the cerebellum (p = 0.01). The concentration of amino acids typical for the hormone-sensitive transport system A was 11% lower during insulin infusion than in the fasting state. CONCLUSION: The uptake of methionine into brain tissue does not seem to be under major control by insulin, while the transport of methionine in the parotid glands is stimulated by insulin. PET provides a sophisticated method to study the transport system of amino acids in vivo.

Hypercaloric glycerol in injured patients.

BACKGROUND: This study investigates the effects of glycerol as a fuel source in the hypermetabolic patient (after injury). METHODS: Twenty-two patients were studied after multiple trauma and randomly assigned to either glucose or glycerol as the carbohydrate source (220 gm glycerol or 320 gm dextrose) during a lipid-based system of parenteral nutrition. In the immediate postoperative period, measurements were made of nitrogen balance, substrates, energy expenditure, insulin, glucagon, and liver function tests. RESULTS: In the glycerol group glucose concentrations in plasma were significantly lower, whereas glycerol levels increased nearly twentyfold. Insulin and glucagon levels increased in both groups; however, the rise in insulin level was greater in the glucose group, whereas glucagon increased in both groups to a similar degree. Nitrogen balance was restored to equilibrium in the glycerol group while remaining negative in the glucose group. No abnormalities in liver function test results or differences in serum albumin levels were noted in either group. A 12% thermic effect was noted in the glucose group but not in the glycerol group. CONCLUSIONS: Glycerol seems to be a viable fuel source in the traumatized patient, being associated with nitrogen retention and minimal thermal effect. A marked rise in plasma levels of glycerol does occur, but this does not appear to have any associated toxicity.

Decreased blood flow but unaltered insulin sensitivity of glucose uptake in skeletal muscle of chronic smokers.

Chronic cigarette smoking is associated with dysfunction of the vascular endothelium. Smokers have also been shown to be insulin-resistant, at least in some studies. Since insulin-induced vasodilation is dependent on endothelial cell nitric oxide (NO) synthesis, we tested the hypothesis that decreased skeletal muscle blood flow causes insulin resistance in smokers. We studied 37 young normotensive normolipidemic nondiabetic men, of which 14 were smokers and 23 lifelong nonsmokers. The groups were similar with respect to age, body mass index (BMI), and maximal oxygen uptake (VO2max). Basal and insulin-stimulated femoral muscle blood flow was measured using [(15)O]H2O and insulin-stimulated muscle glucose uptake using [18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET). Whole-body glucose uptake was measured using the hyperinsulinemic (insulin infusion 5 mU/kg x min)-euglycemic clamp technique. In the basal state, muscle blood flow was 51% lower in smokers (17 +/- 3 mL/kg muscle x min) versus nonsmokers (35 +/- 17 mL/kg x min, P < .0001). Insulin increased muscle blood flow comparably in both groups; the mean rate of insulin-stimulated blood flow was 30 +/- 10 and 55 +/- 38 mL/kg x min (P = .049), respectively. Whole-body and skeletal muscle glucose uptake were similar in both groups during insulin infusion. We conclude that muscle blood flow is lower in chronic smokers compared with nonsmokers under both fasting and hyperinsulinemic conditions. The insulin-induced increase in muscle blood flow and insulin-stimulated glucose uptake appear normal, suggesting that the vasodilatory and metabolic effects of insulin are intact in smokers and the reduced muscle blood flow per se does not cause insulin resistance in these subjects.

Barbiturate anesthesia and brain proton spectroscopy.

BACKGROUND AND PURPOSE: Thiopentone reduces CBF and metabolic rate. Still, it is widely used for sedation during MR spectroscopy. We investigated whether barbiturate anesthesia and preanesthetic fasting have an effect on metabolic ratios in proton MR spectroscopy of the brain. METHODS: Eight healthy, consenting, male volunteers were studied twice in a random, crossover fashion. The study sessions were conducted during fasting (F) and nonfasting (nonF), with glucose infusion mimicking the fed state. During both sessions, two sets of spectroscopic data were collected, one during the awake state (F or nonF) and one under barbiturate anesthesia (F+B or nonF+B), using TEs of 135 and 270. Spectral areas of N-acetylaspartate (NAA), choline-containing compounds (Cho), and creatine plus phosphocreatine (Cr) were calculated, and the presence of lactate or lipid was noted. Venous blood samples for glucose, beta-hydroxybutyrate, lactate, and electrolytes were collected. RESULTS: Barbiturate anesthesia caused a 42% reduction in blood lactate levels during fasting, but not during glucose infusion. There were no differences in NAA/Cho, NAA/Cr, or in Cho/Cr between the groups F, nonF, F+B, or nonF+B. No lactate or lipid resonances were detected. CONCLUSION: Barbiturate anesthesia with preanesthetic fasting can be used for proton spectroscopy at TEs of 135 or 270 without interference from NAA/Cho, NAA/Cr, or Cho/Cr or from the appearance of lactate or lipid.

Failure of additional ketoanalogues of branched chain amino acids to improve the response to parenteral nutrition after experimental trauma in the rat.

The ketoanalogues of branched chain amino acids (KAA) may improve the post-traumatic protein metabolism. We studied the effects of additional KAA, supplied as a part of total parenteral nutrition (TPN), on liver protein synthesis and nitrogen balance in rats after standard surgical trauma. A TPN-regimen, containing 36 mmol/kg/day KAA and 58 mmol/kg/day amino acids was compared to an isonitrogenous (1.0 gN/kg/day) TPN-regimen containing 58 mmol/kg/day amino acids and no KAA in a 48 h experiment. The liver protein synthesis measured by perfusion with C14-leucine in vitro was similar in both groups 2 days after surgery (59.2 +/- 16.2 vs. 64.3 +/- 15.6 arbitrary units, mean +/- SD). The nitrogen balances were negative and of similar magnitude (-0.66 +/- 0.36 vs. -0.17 +/- 0.45 gN/kg/48 h, mean +/- SD). We conclude that TPN supplemented by high supply of KAA offers no systematic advantage over TPN alone after experimental surgical trauma.

Stimulatory effect of glutamine on human monocyte activation as measured by interleukin-6 and soluble interleukin-6 receptor release.

The activation state of murine peritoneal macrophages is shown to depend on extracellular glutamine concentration. However, there are no studies on the effect of glutamine concentration on the activation state of human monocytes. We studied the effect of extracellular glutamine concentration on interleukin (IL-6) and soluble IL-6 receptor (sIL-6R) production by activated monocytes. Monocytes separated by density gradient centrifugation and adherence to glass from buffy coats obtained from healthy donors were activated by 1 pg/ml or 1 ng/ml lipopolysaccharide (LIPS) and incubated for 48 h in 0, 0.1, 0.2, 0.6 and 2.0 mM glutamine. Levels of IL-6 and sIL-6R in culture medium were measured by immunoassay. The extracellular glutamine concentration had a significant effect on IL-6 secretion by activated human monocytes. The mean levels of IL-6 in 0.1 mM glutamine were only marginally higher (P = 0.54) compared to those in the absence of glutamine. A minimum of 0.2 mM glutamine was required to reach the maximal production of IL-6. At all glutamine concentrations the higher concentration of LPS (1 ng/ml) induced higher mean levels of IL-6 than the lower one (1 pg/ml). Glutamine concentration did not affect sIL-6R production. Our results indicate that very low levels of glutamine in plasma may impair the activation of human monocytes as measured by IL-6 secretion.

Metabolic response to experimental trauma: the time relation of post-traumatic protein metabolism.

The relationship between time and the post-traumatic metabolic response was studied in a commonly used experimental model of trauma. Twenty nine rats underwent laparotomy and jugular vein sham catheterization as the standard trauma. The rats were fed ad libitum and compared to pair fed controls in terms of nitrogen balance and liver protein synthesis. The pairs of rats were divided into three groups according to the duration of the experiment, which was 24 h, 48 h or 72 h. The nitrogen balance was calculated daily and the liver protein synthesis in vitro measured in 10 rats after 48 h with an asanguinous perfusion system using L-(1-C(14))-Leucine. The metabolic effect of trauma was first detected in liver protein synthesis, which was diminished in the early post-traumatic period (percentage synthesis rates: post-traumatic 34.6 +/- 10.7 and pair fed 60.4 +/- 21.3, Mean +/- SD, P < 0.05). During this period the whole body nitrogen balances were similar (post-traumatic -1.200 +/- 1.440 and pair fed -0.880 +/- 1.130, gN/kg/48 h, mean +/- SD). On the third day, the response to nitrogen intake and the nitrogen balance became significantly worse in the post-traumatic rats (post-traumatic 0.214 +/- 1.680 and pair fed 1.236 +/- 1.220, gN/kg/day, mean +/- SD). These observations suggest that, firstly, the 'flow' phase has its onset on the third post-trauma day, and secondly that trauma does decrease liver protein synthesis, and this decrease lasts at least through the 'ebb' phase. The results indicate the necessity of defining the metabolic phase in experimental studies of post-traumatic metabolism.

Serum carnitine levels in bone marrow transplant recipients.

This study investigated plasma carnitine levels in patients undergoing allogenic bone marrow transplantation. The patients received fat-based TPN (50% fat, 50% CHO; calorie: nitrogen ratio 125:1) for an average of 33 +/- 7.5 days. TPN was started before transplantation and stopped when patients were able to eat. Caloric needs were estimated using the Harris-Benedict equation; 150% of the estimated BEE was given for the first two weeks after transplantation. The amount of TPN was gradually decreased as patients resumed their oral intake. All patients had low-normal serum carnitine levels before transplantation. There was no significant change in total or free serum carnitine levels during the course of TPN. However, in patients who had symptoms of graft vs. host reaction (GVH), the highest carnitine values during GVH (total 72.3 +/- 6.5 and free 61.2 +/- 12.4 mumol/l) were significantly higher (p < 0.001) than the baseline values (total 27.1 +/- 9.3 and free 24.9 +/- 9.6 mumol/l) or the highest non GVH values after transplantation (total 32.0 +/- 10.7 and free 29.0 +/- 10.7 mumol/l, respectively). The serum triglyceride, total cholesterol, and HDL cholesterol remained within normal range. In conclusion, bone marrow transplant patients receiving fat-based TPN have normal circulating levels of carnitine. GVH reaction caused an increase in the carnitine levels, which was probably due to increased tissue catabolism.

The effect of intermaxillary fixation on leukocyte zinc, serum trace elements and nutritional status of patients undergoing maxillofacial surgery.

Mononuclear cell (MNC), polymorphonuclear cell (PMNC) and serum zinc levels were studied in 17 oral surgical patients with intermaxillary fixation. Serum copper, iron, selenium and bromide concentrations were also measured together with common indices of nutritional status. Nine patients received nutritional counselling. Eight patients had, in addition, oral supplementation with a commercial formula. No changes in intracellular or serum zinc levels were seen during the study period. A statistically significant decrease was seen in mean body weight with subsequent changes in anthropometry. Maximal mean weight loss was 6.0 +/- 3.8% in control group and 3.8 +/- 2.7% in supplemental group. The impaired oral intake due to intermaxillary fixation does not interfere significantly with zinc status as estimated by MNC, PMNC or serum zinc levels. The reduction in body weight and anthropometric indices in the relatively short fixation period may be clinically significant in some patients. Supplementation with a commercial formula helps to maintain the nutritional status of these patients.

Long-term parenteral nutrition in cystic fibrosis.

The effects of parenteral nutrition (PN) with high lipid content were studied in 18 cystic fibrosis patients in this pilot investigation. The patients were randomly assigned to one of two groups. During the first 4-mo period, group 1 received PN and group 2 received routine therapy. During the second 4-mo period, PN was discontinued in group 1 and instituted in group 2. When the effect of PN was considered for both treatment groups, its general effect was to increase body fat content with little or no impact on respiratory function, exercise tolerance, or recurrent infections. However, subsequent analysis and clinical observation suggested that patients receiving PN responded in two seemingly distinct patterns: some demonstrated apparent clinical improvement and benefit, and others did not. A positive response in pulmonary and exercise function was closely correlated to a rise in serum dihomo-gamma-linolenic acid (DHLA) concentrations during PN. Pulmonary function improved in patients who normalized their DHLA levels (vital capacity increased from 2.2 +/- 0.3 to 2.6 +/- 0.3 area %, p < 0.05), whereas those who continued to have undetectable levels of DHLA deteriorated (forced expiratory volume in 1 s decreased from 0.7 +/- to 0.6 +/- 0.1, p < 0.001). PN applied to malnourished patients with cystic fibrosis results in beneficial effects in a subgroup characterized by the presence of DHLA in serum; for the group as a whole, the positive effects are minimal.

Postoperative parenteral nutrition with high supply of branched-chain amino acids: effects on nitrogen balance and liver protein synthesis.

Branched-chain amino acids (BCAA) stimulate muscle and liver protein synthesis in vitro. The significance of this action in catabolic conditions in vivo remains controversial. The effects of a high supply of BCAA in total parenteral nutrition (TPN) on nitrogen balance and liver protein synthesis were studied in a postoperative rat model. After standard operative trauma TPN was commenced with one of two isocaloric programs (I: 20.1% BCAA and II: 50% BCAA) and continued for 48 hr. The relative rate of liver protein synthesis, measured after TPN in vitro by perfusion with 14C-leucine, was similar in both groups (I: 53.4 +/- 17.3 and II: 49.0 +/- 27.3 arbitrary units of synthesis rate, mean +/- SD). The cumulative nitrogen balance was positive with both regimens and was not improved by the high supply of BCAA (I: 2.02 +/- 0.81 and II: 1.87 +/- 0.63 gN/kg/48 hr mean +/- SD). We conclude that after moderate surgical trauma TPN with a high supply of BCAA offers no advantage over conventional TPN.

In situ breakage of a totally implanted venous access system.

Totally implantable systems for venous access are now in wide clinical use. They have been shown to have several advantages when compared with earlier systems. However, the advantages of total implantation also contain risks for new complications. In situ breakages may have disastrous results when unnoticed. In situ separations have been reported with systems consisting of a separate reservoir and catheter. A case is reported where in situ breakage occurred in a system with prefixed catheter. The catheter migrated into pulmonary artery and was removed with Odman catheter and foreign body extractor. The precise cause for the separation could not be ascertained. It is emphasized that during insertion the silicone catheter should not be handled with surgical instruments and that the continuity of the system should be checked prior to use.

The effects of branched chain amino acid infusion on pain perception and plasma concentrations of monoamines.

Infusions of branched chain amino acids (BCAA) have been shown to have several CNS-mediated effects including antinociceptive action. We investigated the effects of BCAA infusion on pain perception, respiratory control, and plasma monoamine concentrations. Six healthy female volunteers were given in a double-blind, random, crossover design an 8-h infusion (1.75 ml/kg/h) of either (a) Ringers lactate, (b) conventional 4% amino acid solution, or (c) 4% BCAA solution with intervals of at least 48 h. Respiratory control was evaluated with continuous capnography. Pain perception was measured using dental dolorimetry for sharp pain, and pain transmitted by afferent C-fibers was evaluated with tourniquet test. Changes in vigilance were measured using critical flicker fusion technique. Evaluations were made for baseline, and after 2.5, 5, and 8 h. Plasma samples were collected at the same time points for amino acid and monoamine analysis. BCAA infusion resulted in significant increases of plasma concentrations of all BCAAs, with a simultaneous decrease in concentrations of aromatic amino acids. Of the measured monoamines and their metabolites dihydroxyphenylacetic acid (DOPAC) decreased, showing significant treatment effect for BCAA. Despite these changes no significant effect of BCAAs on respiratory control, vigilance, or pain perception was observed. In conclusion, despite significant changes in plasma concentrations of both amino acids and DOPAC, BCAA infusion did not show any clinically relevant antinociceptive effect.