Cardiac troponin T content in heart and skeletal muscle and in blood samples from ApoE/LDL receptor double knockout mice.

BACKGROUND: The isolated perfused mouse heart is a useful experimental model, and cardiac troponin T (cTnT) in coronary effluent may be a sensitive marker of myocardial damage. In recent years, the apolipoprotein E/low-density lipoprotein receptor double knockout (apoE/LDLr KO) mice have become valuable tools in atherosclerosis research. The aim of the study was to validate measurements of cTnT in heart, skeletal muscle, and serum of apoE/LDLr KO mice. METHODS: Wild-type C57BL/6J mice were fed with standard diet, and apoE/LDLr KO mice were fed an atherogenic diet. Blood was sampled from the jugular vein or the thoracic cavity. Heart and femoral skeletal muscle were sampled and homogenized. cTnT was measured with the third-generation cTnT assay (Troponin T STAT) on Elecsys 2010 immunoassay analyser (Roche Diagnostics). RESULTS: Median serum cTnT in samples from the thoracic cavity of C57BL/6J mice was about 20-90 times higher, and from ApoE/LDLr KO mice about 30 times higher than serum cTnT in samples from the external jugular vein. There was no difference in cTnT content (microg cTnT/g heart muscle) in hearts from C57BL/6J and apoE/LDLr KO mice. The median cTnT content in skeletal muscle was less than 0.1% of the cTnT content in heart muscle. CONCLUSION: There is no difference in cTnT content of heart muscle comparing C57BL/6J and ApoE/LDLr KO mice, which have larger hearts. Sampling from the thoracic cavity causes unacceptably high cTnT levels. Serum cTnT in samples from the jugular vein is only slightly elevated. Elevated baseline levels of cTnT in mice are not caused by troponin T from skeletal muscle.

Effects on skeletal muscle of intravenous glutamine supplementation to ICU patients.

OBJECTIVE: To evaluate the effect of four doses of intravenous glutamine supplementation on skeletal muscle metabolism. DESIGN: A prospective, blinded, randomized study. SETTING: The general Intensive Care Unit (ICU) of a university hospital. PATIENTS: ICU patients with multiple organ failure (n=40), who were expected to stay in the unit for more than five days. INTERVENTION: Patients received 0, 0.28, 0.57 or 0.86 g of glutamine per kg bodyweight per day intravenously for five days as part of an isocaloric, isonitrogenous and isovolumetric diet. RESULTS: Plasma glutamine concentration responded to glutamine supplementation with normalization of plasma levels in a dose-dependent way, while free muscle glutamine concentration, as well as muscle protein synthesis and muscle protein content, did not change significantly. CONCLUSION: Intravenous glutamine supplementation to ICU patients for a period of five days resulted in normalization of plasma glutamine concentrations in a dose-dependent way whereas muscle glutamine concentrations were unaffected.

Free amino acids in plasma, red blood cells, polymorphonuclear leukocytes, and muscle in normal and uraemic children.

BACKGROUND: The aims of this study were to investigate free amino acid (AA) concentrations in plasma, red blood cells (RBC), polymorphonuclear granulocytes (PMN), and muscle, sampled at the same time, in normal and uraemic children. METHODS: Twelve apparently well-nourished chronically uraemic children (five females) aged a mean of 9.4+/-4.8 (range 1.7--17.7) years and 13 age-matched normal children were studied. Venous blood and muscle samples for AA analyses were taken simultaneously after an overnight fast. RESULTS: The intracellular AA patterns in the three cellular compartments were qualitatively similar, but the absolute intracellular concentrations were higher in muscle than in PMN, which had higher values than in RBC. The AA patterns in plasma, RBC, PMN, and muscle in the uraemic children have many similarities; typical features being low branched-chain AA (BCAA), tyrosine, and serine concentrations and variably high concentrations of some non-essential AA. Among the individual AA, there were only few correlations between their concentrations in the three cell compartments. CONCLUSIONS: The lack of correlation between the concentrations in RBC, PMN, and muscle for most of the AA indicates that there is no close association in the same subject between individual free AA concentrations in various types of cells, presumably because of differences in metabolism and function. Consequently, one should be cautious in assuming that AA concentrations, determined in RBC or PMN, reflect the concentrations in muscle cells. Therefore, these preliminary observations do not support the hypothesis that RBC and PMN AA analysis can be considered as a suitable alternative to muscle AA determination.