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Biomedical subjects

Jan Wernerman

Publications and source records attributed to Jan Wernerman.

27 records · Page 2Linked to original sources
PubMed2002

Nutritional papers in ICU patients: what lies between the lines?

The abundance of literature related to nutritional support reflects its recently recognised role in preventing metabolic complications and gut dysfunction during critical illness. However, some published studies lack relevance to critically ill patients, as a result of the selection of subjects and outcome variables, or flaws in the study design, as well as in the type, composition, timing, route of administration and amount of nutritional support given. This review will highlight these confounding factors by describing two imaginary (but typical) clinical trials and by analysing some studies published. The point at issue is that basic quality requirements, such as the formulation of a prospective hypothesis and the delineation of the effects of the reference treatment, are often lacking in many studies published. Data analysis was often found to be biased by the absence of statistical power calculation and intention-to-treat analysis. Globally, studies designed to assess the effects of nutritional support on the outcome of critically ill patients, rarely fulfil basic quality requirements and should therefore be interpreted cautiously. We suggest simple strategies or study design that will allow important questions to be answered by future clinical trials.

Clinical Trials as Topic↗
PubMed2002

Position paper of the ESICM Working Group on Nutrition and Metabolism. Metabolic basis of nutrition in intensive care unit patients: ten critical questions.

The metabolic changes associated with critical illness involve several pathways acting at different steps of the utilization of nutritive substrates. The understanding of the role of these pathways and of their complex regulation has led to the development of new strategies for the metabolic and nutritional management of critically ill patients, including the development of new products for nutritional support. The rationale for changing the profile of nutritional support solutions by adding novel substrates is also discussed. This review focuses on the metabolic specificities of critically ill patients and also includes an analysis of the adequacy of tools to monitor the metabolic status and the adequacy of the nutritional support.

Critical Care↗
PubMed2002

Glucose flux is normalized by compensatory hyperinsulinaemia in growth hormone-induced insulin resistance in healthy subjects, while skeletal muscle protein synthesis remains unchanged.

The aim of this present investigation was to study the relationship between the reduction in insulin sensitivity accompanying 5 days of treatment with growth hormone (GH; 0.05 mg.24 h(-1).kg(-1)) and intracellular substrate oxidation rates in six healthy subjects, while maintaining glucose flux by a constant glucose infusion and adjusting insulin infusion rates to achieve normoglycaemia (feedback clamp). Protein synthesis rates in skeletal muscle (flooding dose of L-[(2)H(5)]phenylalanine) were determined under these conditions. We also compared changes in insulin sensitivity after GH treatment with simultaneous changes in energy requirements, protein synthesis rates, nitrogen balance, 3-methylhistidine excretion in urine, body composition and the hormonal milieu. After GH treatment, 70% more insulin was required to maintain normoglycaemia (P<0.01). The ratio between glucose infusion rate and serum insulin levels decreased by 34% at the two levels of glucose infusion tested (P<0.05). Basal levels of C-peptide, insulin-like growth factor (IGF)-I and IGF-binding protein-3 increased almost 2-fold, while levels of glucose, insulin, glucagon, GH and IGF-binding protein-1 remained unchanged. Non-esterified fatty acid levels decreased (P<0.05). In addition, 24 h urinary nitrogen excretion decreased by 26% (P<0.01) after GH treatment, while skeletal muscle protein synthesis and 3-methylhistidine excretion in urine remained unchanged. Energy expenditure increased by 5% (P<0.05) after treatment, whereas fat and carbohydrate oxidation were unaltered. In conclusion, when glucose flux was normalized by compensatory hyperinsulinaemia under conditions of GH-induced insulin resistance, intracellular rates of oxidation of glucose and fat remained unchanged. The nitrogen retention accompanying GH treatment seems to be due largely to improved nitrogen balance in non-muscle tissue.

Adult↗
PubMed2002

Albumin synthesis in humans increases immediately following the administration of endotoxin.

In order to investigate the immediate (i.e. within 3 h) response of albumin synthesis to the administration of endotoxin, as a model of a moderate and well controlled catabolic insult, two measurements employing L-[(2)H(5)]phenylalanine were performed in 16 volunteers. One group ( n =8) received an intravenous injection of endotoxin (4 ng/kg; lot EC-6) immediately after the first measurement of albumin synthesis, whereas the other group received saline. A second measurement was initiated 1 h later. In the endotoxin group, the fractional synthesis rate of albumin was 6.9+/-0.6%/day (mean+/-S.D.) in the first measurement. In the second measurement, a significant increase was observed (9.6+/-1.2%/day; P <0.001). The corresponding values in the control group were were 6.6+/-0.6%/day and 7.0+/-0.6%/day respectively (not significant compared with first measurement and P <0.001 compared with the second measurement in the endotoxin group). The absolute synthesis rates of albumin were 148+/-35 and 201+/-49 mg x kg(-1) x day(-1) before and after endotoxin ( P <0.01). In the control group, the corresponding values were 131+/-21 and 132+/-20 mg x kg(-1) x day(-1) (not significant compared with the first measurement and P <0.01 compared with the second measurement in the endotoxin group). In conclusion, these results indicate that albumin synthesis increases in the very early phase after a catabolic insult, as represented by the administration of endotoxin.

Adult↗
PubMed2002

Metabolic changes in the liver graft monitored continuously with microdialysis during liver transplantation in a pig model.

Microdialysis provides the opportunity to continuously monitor metabolic changes in tissue. The aim of the study is to monitor metabolic changes in the liver graft over time during transplantation in a pig model. Fourteen littermate female pigs with a body weight of 30 to 34 kg were used for seven orthotopic liver transplantations. Intrahepatic implantation of a microdialysis catheter into the liver graft was performed in the donor. Microdialysis samples were collected at 20-minute intervals during the donor operation, cold preservation, and for 7 hours after reperfusion in the recipient. Glucose, lactate, pyruvate, and glycerol concentrations were measured. After cold perfusion, glucose, lactate, and glycerol levels increased, whereas pyruvate levels decreased rapidly. During cold storage, glucose and glycerol levels increased, whereas lactate levels remained stable and pyruvate levels were undetectable. During implantation of the liver graft, glucose, lactate, and glycerol levels showed an accelerated increase. After portal reperfusion, glucose, lactate, and glycerol levels continued to increase for another 40 to 60 minutes, after which they decreased and finally settled at normal levels. At this time, pyruvate levels increased, with a peak within 2 hours after reperfusion, and then decreased to normal levels. Calculated lactate-pyruvate ratio increased after cold perfusion and remained stable during cold storage. During rewarming, it showed an accelerated increase, but after reperfusion, it decreased rapidly. Rewarming and reperfusion are most harmful to the liver, reflected by an accelerated increase in glucose and glycerol levels and lactate-pyruvate ratio. High intrahepatic glucose levels during ischemia appear to be a liver-specific event, which may represent glycogen degradation in injured hepatocytes.

Animals↗
PubMed2002

Bacterial translocation: effects of artificial feeding.

The most striking observation when reviewing recent literature in the field of bacterial translocation in the intestine is the small number of publications involving human subjects. Although there are some excellent reviews in this field published during the last 2 years, all experimental contributions come from animal experiments. It is therefore crucial to evaluate how valid the animal models are for human pathophysiology. Studies focusing on translocation as a major pathogenic mechanism are urgently needed to help clinicians to make correct decisions concerning protection of the gut and decide upon nutrition in the intensive care unit.

Animals↗