| 1. |
- Nettelbladt, C. G., et al.
(author)
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Starvation increases the number of coliform bacteria in ceacum and induces bacterial adherence to caecal epithelium in rats
- 1997
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In: European Journal of Surgery. - Stockholm, Sweden : Taylor & Francis. - 1102-4151 .- 1741-9271. ; 163:2, s. 135-142
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Journal article (peer-reviewed)abstract
- Objective: To investigate the impact of starvation for 24 and 48 h on the number of coliform bacteria in the caecal contents, on the mucosal adherence of coliform bacteria, and on bacterial translocation in rats.Design: Open prospective study.Setting: University departments of surgery and microbiology, Sweden.Material: 46 adult male Sprague-Dawley rats.Interventions: 19 rats served as controls, and were fed until samples were taken. Six animals were starved for 24 h and another 15 for 48 h, with free access to water, and then anaesthetised before blood, mesenteric lymph nodes (MLN), caecum, and caecal contents were sampled. To verify bacterial translocation in this strain of rats, another six rats underwent controlled haemorrhage for 60 min to reduce the blood pressure to 55 mm Hg mean arterial pressure (MAP). These rats had free access to food and water before haemorrhage but were allowed only water until samples were taken 24 h after haemorrhage.Main Outcomes Measures: Presence and number of coliform bacteria in samples taken from caecal contents, caecal epithelium, MLN, and blood.Results: Starvation for 24 h increased the number of coliform bacteria (colony forming units (CFU)/g) in the caecal contents 25-fold (p < 0.05). Starvation for 48 h further increased the number by a factor of 100. The number of coliform bacteria that adhered to the caecal epithelium increased 3,000 times in rats that had been starved for 48 h (p < 0.001). There was no significant difference in translocation (as indicated by cultures from MLN) between rats that had been fed and those that had been starved for 48 h. In 4 of the 6 rats that were bled and then starved for 24 h there were signs of bacterial translocation, which was significantly more than the 1/19 in fed rats (p < 0.05).Conclusion: Starvation increases the number of bacteria in the caecal contents and increases bacterial adherence to the caecal epithelium. These changes may contribute to the previously reported increase in bacterial translocation in starved compared wit fed rats that were subjected to stress. The same changes in the gut were observed in animals subjected to haemorrhagic stress in addition to starvation, and in which bacterial translocation was evident.
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| 2. |
- Balagopal, P., et al.
(author)
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Skeletal muscle heavy-chain synthesis rate in healthy humans
- 1997
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In: American Journal of Physiology. - : HighWire Press. - 0002-9513 .- 2163-5773. ; 272:1, s. 45-50
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Journal article (peer-reviewed)abstract
- Mixed muscle protein synthetic rate has been measured in humans. These measurements represent the average of synthetic rates of all muscle proteins with variable rates. We determined to what extent the synthesis rate of mixed muscle protein in humans reflects that of myosin heavy chain (MHC), the main contractile protein responsible for the conversion of ATP to mechanical energy as muscle contraction. Fractional synthetic rates of MHC and mixed muscle protein were measured from the increment of [C-13]leucine in these proteins in vastus lateralis biopsy samples taken at 5 and 10 h during a primed continuous infusion of L-[1-C-13]leucine in 10 young healthy subjects. Calculations were done by use of plasma [C-13]ketoisocaproate (KIC) and muscle tissue fluid [C-13]leucine as surrogate measures of leucyl-tRNA. Fractional synthetic rate of MHC with plasma KIC (0.0299 +/- 0.0043%/h) and tissue fluid leucine (0.0443 +/- 0.0056%/h) were only 72 +/- 3% of that of mixed muscle protein (0.0408 +/- 0.0032 and 0.0603 +/- 0.0059%/h, respectively, with KIC and tissue fluid leucine). Contribution of MHC (7 +/- 1 mg . kg(-1) . h(-1)) to synthetic rates of whole body mixed muscle protein (36 +/- 5 mg . kg(-1) . h(-1)) and whole body protein (127 +/- 4 mg . kg(-1) . h(-1)) is only 18 +/- 1 and 5 +/- 1%, respectively. This relatively low contribution of MHC to whole body and mixed muscle protein synthesis warrants direct measurement of synthesis rate of MHC in conditions involving abnormalities of muscle contractile function.
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| 3. |
- Gannerdahl, Per E., et al.
(author)
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Comparison of electrocardiograms recorded with standardleads and derived from the vectorcardiographic frank leads in high risk patients
- 1997
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In: Intensive Care Medicine. - : Springer Science and Business Media LLC. - 0342-4642 .- 1432-1238. ; 23:10, s. 1049-1055
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Journal article (peer-reviewed)abstract
- Dynamic vectorcardiography (VCG) is increasingly employed for ischaemia monitoring with the use of a computerized method for recording and on-line analysis by the calculation of trend parameters. To elucidate how well the derived electrocardiogram (dECG), calculated from the VCC, compares with the simultaneously registered standard ECG (sECG), dECGs from 17 postoperative cardiac-risk patients and 36 subjects with acute myocardial infarction (AMI) were compared to sECGs, both quantitatively in leads II, III, V2 and V5 and qualitatively. Despite small, but some significant differences, mainly in the amplitudes of precordial leads, the qualitative interpretation by two independent cardiologists showed good agreement between the methods (kappa = 0.72 and 0.67, respectively) for the diagnosis of AMI/ischaemia. The dECG seems to be reliable and can be used clinically in these groups of patients during VCG recordings.
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| 4. |
- Gannerdahl, Per E., et al.
(author)
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Vectorcardiographic changes during laparoscopiccholecystectomy may mimic signs of myocardial ischaemia
- 1997
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In: Acta Anaesthesiologica Scandinavica. - : Elsevier. - 0001-5172 .- 1399-6576. ; 41:9, s. 1187-1192
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Journal article (peer-reviewed)abstract
- Laparoscopic surgery involves the use of intra-abdominal carbon dioxide insufflation (pneumoperitoneum). The increased intra-abdominal pressure causes marked haemodynamic changes, which may influence electrocardiographic monitoring. The aim of the present study was to elucidate the influence of pneumoperitoneum on vectorcardiographic recordings.METHODS:Vectorcardiographic changes (QRS vector difference = QRS-VD, QRS loop area, QRS magnitude, ST vector magnitude, spatial ST vector change) were recorded continuously applying computerized vectorcardiography in 12 anaesthetised cardiovascularly healthy patients, scheduled for laparoscopic cholecystectomy. Measurements were made before and during pneumoperitoneum in three different body positions (supine, Trendelenburg and reversed Trendelenburg), also employing transesophageal echocardiography and invasive blood pressure monitoring.RESULTS:Pneumoperitoneum significantly increased QRS-VD, in parallel with an enlargement in loop area and magnitude. The magnitude was significantly increased in the transversal and frontal planes and there was a tendency to increase the magnitude in the sagittal plane. The increase in QRS-VD reached levels previously associated with the development of myocardial ischaemia in patients with coronary artery disease. The ST-variables were not changed by the pneumoperitoneum. The positional changes also influenced QRS-VD significantly.CONCLUSIONS:When computerized vectorcardiography is used for ischaemia monitoring during pneumoperitoneum, the ST-variables seem reliable. However, vectorcardiographicQRS-changes should be interpreted with caution, as the QRS alterations found during pneumoperitoneum mimic the changes seen during myocardial ischaemia.
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| 5. |
- Ljungqvist, Olle, 1954-, et al.
(author)
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Functional heterogeneity of leucine pools in human skeletal muscle
- 1997
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In: American Journal of Physiology. - : HighWire Press. - 0002-9513 .- 2163-5773. ; 273:3 Pt 1, s. E564-E570
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Journal article (peer-reviewed)abstract
- Current models to measure muscle protein synthesis in humans assume a homogeneous intracellular amino acid pool. This assumption was tested by measuring the isotopic enrichment of leucine and its transamination product alpha-ketoisocaproate (KIC) in plasma and muscle tissue fluid and comparing them with that of leucyl-tRNA during a continuous infusion of L-[1-13C]leucine in 12 healthy subjects. Six subjects were studied twice while drinking a carbohydrate (0.42 kcal/kg) drink every 20 min for 11 h or the same volume of water. Six others took an isocaloric mixed meal providing 14 mg protein/kg every 20 min and water. Enrichment of plasma and tissue fluid KIC and plasma leucine was consistently higher than that of leucyl-tRNA and tissue fluid leucine (P < 0.01), whereas the enrichment of leucyl-tRNA was equivalent to that of tissue fluid leucine in all experiments. Furthermore, the ratio of enrichment of leucyl-tRNA to that of plasma leucine and KIC decreased after the mixed meal, whereas that of leucyl-tRNA to tissue fluid leucine remained constant. The enrichment of KIC was closer (approximately 17% lower) to that of plasma leucine than that of leucyl-tRNA (approximately 43% higher), indicating that the transamination pool derived more leucine from extracellular sources than the acylation pool. We conclude that the use of plasma KIC enrichment as a surrogate measure of leucyl-tRNA enrichment substantially underestimates muscle protein synthetic rates in humans, whereas tissue fluid leucine enrichment is a valid surrogate measure. In addition, the differences in enrichment of leucyl-tRNA and KIC support a regulated cytoplasmic trafficking of leucine in muscle cells.
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| 6. |
- Nygren, Jonas, et al.
(author)
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Short-term hypocaloric nutrition but not bed rest decrease insulin sensitivity and IGF-I bioavailability in healthy subjects : the importance of glucagon
- 1997
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In: Journal of Nutrition. - : Oxford University Press. - 0022-3166 .- 1541-6100. ; 13:11-12, s. 945-951
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Journal article (peer-reviewed)abstract
- Hyperinsulinemic, normoglycemic clamps were performed before and after 24 h of either hypocaloric nutrition or bed rest in healthy subjects. Decreased insulin sensitivity and insulin-like growth factor-I (IGF-I) bioavailibility, as measured by the serum IGF-I/insulin-like growth factor binding protein-1 (IGFBP-1) ratio, was found after fasting, whereas no metabolic changes were found after bed rest. Glucagon seems to be a key regulator of IGFBP-1 after brief hypocaloric nutrition. Hypocaloric nutrition and immobilization may add to the catabolic response to surgery and other trauma. Presently, six healthy subjects were studied before and after a 24-h period of hypocaloric nutrition (200 kcal/24 h, fast) or immobilization (bed rest) using the hyperinsulinemic (0.8 mU · kg−1 · min−1), normoglycemic (4.5 mmol/L) clamp, indirect calorimetry, and circulating levels of substrates and hormones. After fast, body weight decreased (P < 0.05), and nitrogen balance was negative (−10 ± 1 g urea nitrogen/24 h). Basal levels of free fatty acids, glucagon, and IGFBP-1 increased (P < 0.05), whereas c-peptide levels and the IGF-I/IGFBP-1 ratio decreased (P < 0.05). However, no change was found in basal levels of IGF-I or substrate oxidation. Furthermore, changes (%) in basal levels of glucagon after fast correlated to IGFBP-1 (r = 1.0, P < 0.05), whereas the suppressibility of IGFBP-1 by insulin was maintained at normal levels. During clamps, glucose infusion rates (GIR) decreased after fast (−43 ± 13%, mean ± SEM, P < 0.001). Although not significant, clamp levels of fat oxidation tended to increase and glucose oxidation tended to decrease. Levels of IGFBP-1 during clamps were higher as compared with the control clamp (P < 0.05). No adverse metabolic changes were seen after bed rest, and no change in GIR during clamps were seen as compared with the control measurement (0 ± 14%). After brief hypocaloric nutrition, insulin sensitivity is reduced, whereas IGF-I bioavailibility is reduced by an increase in levels of IGFBP-1. Glucagon seems to contribute to the increase in IGFBP-1 during these conditions.
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| 7. |
- Nygren, Jonas, et al.
(author)
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Site of insulin resistance after surgery: : the contribution of hypocaloric nutrition and bed rest.
- 1997
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In: Clinical Science. - : Portland Press. - 0143-5221 .- 1470-8736. ; 93:2, s. 137-146
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Journal article (peer-reviewed)abstract
- Insulin resistance after surgery has been shown to be related to several important derangements in protein and fat metabolism. However, mechanisms of impaired glucose tolerance after surgery remain ill-defined. 2. Insulinsensitivity and glucose (6,62H2-glucose) were studied in seven before and after elective surgery (surgery group), by two step-hyperinsulinaemic (0.3 and 0.8 munits kg-1min-1), normoglycaemic (4.5 mmol/l) clamps. Six healthy subjects were studied, using the same protocol, before and after a similar period of bed rest and hypocaloric nutrition (fast/bed rest group) to delineate the effects of surgery per se. 3. Basal endogenous glucose production and whole-body glucose disposal was higher after surgery (P < 0.001), whereas no change was found after fast/bed rest. During glucose clamps, the glucose infusion rates required to maintain normoglycaemia and whole-body glucose disposal decreased (P < 0.001) after surgery, while endogenous glucose production increased (P < 0.001). In the control subjects, levels of endogenous glucose production remained unchanged after fast/bed rest. In contrast, glucose infusion rates and whole-body glucose disposal during glucose clamps also decreased after fast/bed rest (P < 0.01). However, the relative decrease in both these parameters was greater after surgery compared with after fast/bed rest (P < 0.01). 4. After surgery, energy expenditure and fat oxidation increased (P < 0.001), whereas glucose oxidation decreased (P < 0.05). No significant change was found in glucose utilization postoperatively. After fast/bed rest, no change was found in energy expenditure. However, fat oxidation increased (P < 0.01), whereas glucose oxidation and glucose utilization decreased (P < 0.05). 5. In conclusion, impaired glucose tolerance develops after surgery as a result of decreased insulin-stimulated whole-body glucose disposal as well as increased endogenous glucose release. Despite the increase in endogenous glucose production, the reduction in endogenous glucose production with each elevation of insulin was unaffected by surgery. Perioperative bed rest and/or hypocaloric nutrition contributed to the decrease in insulin-stimulated whole-body glucose disposal in the postoperative state, whereas these factors have no effects on endogenous glucose production.
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