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Biomedical subjects

G Garibotto

Publications and source records attributed to G Garibotto.

At least 37 records · Page 2Linked to original sources
PubMed1996

Muscle protein turnover in chronic renal failure patients with metabolic acidosis or normal acid-base balance.

It is currently unknown if metabolic acidosis has any effect on muscle protein metabolism in patients with chronic renal failure (CRF). To address this question, muscle protein turnover was studied in patients with CRF and controls in the postabsorptive state by using the forearm perfusion method together with the 3H-phenylalanine kinetics. Nine patients were acidotic ([HCO-3]a = 20 +/- 0.5 mEq/l) whereas 4 patients had a normal acid-base balance ([HCO-3]a = 25 +/- 0.3 mEq/l). In patients with metabolic acidosis the rates of phenylalanine appearance and disposal from the forearm were increased as compared to controls. Phenylalanine net balance, i.e. net proteolysis, was only slightly higher than in controls. In patients under a normal acid-base balance both rates of appearance and disposal of phenylalanine as well as phenylalanine net balance were similar to controls. These preliminary data suggest that metabolic acidosis can enhance the rate of muscle protein degradation in patients with CRF.

Acidosis↗
PubMed1995

Robot-assisted microscope for neurosurgery.

We describe the implementation of a robotic arm connected to a neurosurgical operative microscope. A force feedback sensor drives the motors of the arm in response to the positioning of the microscope by the surgeon. Computer graphic techniques allow tracking of the current position of the microscope within the volumetric reconstruction of the brain. The integration of the prototype into the neurosurgical operating room is currently being evaluated. Preliminary comments on this experimental phase are offered.

Angiography, Digital Subtraction↗
PubMed1995

Disposal of exogenous amino acids by muscle in patients with chronic renal failure.

Muscle exchange of amino acids (AAs) was evaluated by using the arteriovenous-difference technique across the leg in seven patients with chronic renal failure (CRF) and eight control subjects before and for 75 min after the ingestion of an AA mixture simulating an animal-protein meal. Total AAs increased in arterial blood much more in patients with CRF after AA ingestion than in control subjects, as a consequence of an exaggerated increase in nonessential AAs (NEAAs) (+127%). Moreover, total AAs were taken up by the leg in larger amounts than in control subjects (+71%, P < 0.0025) because of increased uptake of NEAAs (+156%, P < 0.005). Branched-chain AA uptake by the leg was, in absolute values, similar to that of control subjects; however, because of the increased uptake of total AAs, branched-chain AA uptake was only 30% of total AA extraction, compared with 46% in control subjects. Abnormalities in AA uptake by muscle paralleled those in arterial AAs. In fact the same AAs that increased abnormally in blood were taken up by the leg at higher rates than in control subjects. Variations in arterial concentrations and muscle uptake of AAs were inversely related to arterial bicarbonate concentration, suggesting a role for acid-base status in modifying both the arterial supply and muscle metabolism of AAs. Results indicate that in CRF patients the normal pattern of postprandial AA repletion is disrupted. Muscle tissue faces the increased and unbalanced postprandial supply of AAs with an augmented and unbalanced uptake. Data are consistent with an abnormal use of exogenous AAs in CRF patients, possibly induced by metabolic acidosis.

Adult↗
PubMed1994

Skeletal muscle protein synthesis and degradation in patients with chronic renal failure.

Muscle protein turnover and amino acid (AA) exchange across the forearm were studied in nine postabsorptive patients with chronic renal failure (CRF) under unrestricted calorie-protein diets and eight controls by using the arterio-venous difference technique associated with the 3H-phenylalanine kinetics. In patients with CRF: (1) the rate of appearance (Ra) of phenylalanine (Phe) from the forearm, reflecting proteolysis, was 27% increased in comparison with controls (P < 0.01). Also the rate of disposal (Rd) of Phe, reflecting protein synthesis, was increased in patients (P < 0.01). As a consequence of these counterbalanced alterations, net balance of Phe across the forearm, that is, net proteolysis, was not changed. (2) The release of total AA from the forearm was not different from controls. Valine and ketoisocaproate release was reduced (P < 0.05). Serine uptake was not detectable. (3) Net proteolysis and the Rd/Ra ratio were inversely and directly, respectively, related to arterial [HCO3-] (P < 0.02 and P < 0.03, respectively). (4) Moreover, net proteolysis and Phe Rd/Ra ratio were directly and inversely, respectively, correlated with plasma cortisol (P < 0.01 and < 0.005, respectively). Plasma cortisol was in the normal range and inversely related to arterial [HCO3-] (P < 0.02). (5) While in controls phenylalanine appearance from the forearm was inversely related to insulin levels, no correlation was found in patients. In conclusion, in patient with CRF, forearm Phe kinetics indicate the existence of an increased muscle protein turnover. Changes in protein synthesis and degradation are well balanced and net proteolysis is not augmented.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Role of haematological, pulmonary and renal complications in the long-term prognosis of patients with lysinuric protein intolerance.

Three patients with lysinuric protein intolerance are reported. The first patient displayed severe haemolytic anaemia, bone marrow erythroblastophagocytosis, renal tubular disease and interstitial lung disease. Despite treatment with citrulline and low-protein diet, this child died at the age of 18 months. The second patient is now 24 years old and has chronic interstitial lung disease and focal renal glomerulosclerosis. The third patient, now 5 years old, has severe chronic interstitial lung disease. A 6-month treatment with prednisone was ineffective in the second and third patients.

Adolescent↗
PubMed1993

Effects of a protein meal on blood amino acid profile in patients with chronic renal failure.

Arterial whole blood levels of amino acids were determined in patients with chronic renal failure and in healthy subjects before and after 270 min after the ingestion of a grilled beefsteak (4 g/kg). In patients, total nonessential amino acids increased significantly more (+46%) than in controls owing to an exaggerated rise of serine, glutamine, proline, glycine, cyst(e)ine and alanine. Total essential amino acids increased as much as in controls; however, threonine, histidine and phenylalanine showed greater increases, while tryptophan had a smaller increment. Abnormalities in amino acid levels were even more evident in the postprandial period than in the postabsorptive state owing to reduced levels of valine, leucine, tryptophan, tyrosine, aspartate and glutamate and higher levels of glutamine, proline, glycine, cyst(e)ine, threonine, histidine and phenylalanine. Moreover, after the meal, the ratios total essential amino acids/total nonessential amino acids, valine/glycine, and branched-chain amino acids/total amino acids rose but persisted to be reduced whereas tryptophan/total amino acids and tyrosine/phenylalanine ratios increased in controls, but did not change in patients. In conclusion, in chronic renal failure, protein ingestion enhances the imbalance in amino acid levels already present in the postabsorptive state. The all data indicate that in patients with chronic renal failure, the metabolism of exogenous protein is impaired and the flow of amino acids to the organs is altered during the phase of body nitrogen replenishment.

Adult↗
PubMed1993

Erythropoietin treatment and amino acid metabolism in hemodialysis patients.

A previous report suggests that treatment with recombinant human erythropoietin (rH-EPO) significantly improves many abnormalities in circulating amino acids (AA) in hemodialysis patients. We evaluated the effects of a 12-month treatment with rH-EPO (150-250 U/kg/week) on blood AA levels in 10 patients with chronic renal failure under regular dialytic treatment. During treatment, hemoglobin levels increased from 7.0 +/- 0.3 to 10.1 +/- 0.3 g/dl at 3 months remaining steady thereafter. Before the treatment, patients showed reduced levels of essential AA (EAA), mainly valine, leucine and threonine (p < 0.05-0.01); among non-EAA (NEAA), aspartate and serine were reduced, whereas glycine, alanine, proline, citrulline and cyst(e)ine were increased (p < 0.05-0.001). Val/Gly, Ser/Gly and Tyr/Phe ratios were low (p < 0.05-0.01). Total EAA and total NEAA (619 +/- 21 and 1,382 +/- 75 mumol/l, respectively, before the study) were unchanged (639 +/- 22 and 1,410 +/- 89 mumol/l, respectively) at 12 months. Abnormalities in AA levels observed before the treatment persisted throughout the study. Only serine increased at the end of the study (p < 0.05). In conclusion, contrary to what has been reported, treatment with rH-EPO is not associated with an amelioration of AA metabolism in hemodialysis patients.

Adult↗
PubMed1993

Peripheral metabolism of branched-chain keto acids in patients with chronic renal failure.

Peripheral tissue metabolism of branched-chain amino acids (BCAA) and branched-chain keto acids (BCKA) in the postabsorptive state was evaluated in 8 patients with chronic renal failure (CRF) and 7 controls by measuring the arterial-deep forearm venous differences for BCAA and BCKA. Arterial whole blood levels of BCAA and BCKA were also measured in an additional 7 patients and 11 controls. In CRF, total BCKA levels are reduced owing to a decrease in ketoisocaproic acid (KICA) and ketoisovaleric acid (KIVA) levels, parallel to changes in BCAA levels, whereas levels of ketomethylvaleric acid (KMVA) are not different from controls. Both in normal conditions and in patients, arterial levels of individual BCAA are directly correlated with arterial levels of the corresponding BCKA. However, in CRF, the ratios of leucine to KICA and of isoleucine to KMVA are increased. A direct correlation between KICA and HCO3- levels is observed. In CRF, the release of leucine and valine as well as of KICA and KMVA from peripheral tissues is reduced, whereas KIVA is neither released nor taken up by the forearm. The lack of KICA release from peripheral tissues likely accounts for its low circulating levels. The depressed peripheral release of leucine associated with the lack of KICA release suggests an increased degradation of leucine which proceeds beyond the transamination step.

Adult↗
PubMed1992

Muscle protein turnover and amino acid metabolism in patients with chronic renal failure.

Muscle protein turnover and amino acid (AA) exchange were studied in 4 patients with chronic renal failure (CRF) and in 5 controls in the postabsorptive state by using the forearm perfusion method together with the systemic infusion of 3H-Phe. In CRF patients muscle protein breakdown is increased and is associated with a parallel increase in protein synthesis. Protein breakdown is inversely related to arterial bicarbonate. Net proteolysis is unchanged. The release of total AA, glutamine and alanine is not different from controls, whereas the release of valine and leucine is reduced and serine uptake tends to be decreased. In conclusion, in postabsorptive patients with CRF, well before the uremic stage, an increased protein breakdown associated with metabolic acidosis takes place; net proteolysis is unaffected. Alterations in BCAA metabolism suggest the occurrence of increased BCAA degradation proceeding beyond the transamination step.

Adult↗
PubMed1991

Reversed-phase high-performance liquid chromatographic analysis of branched-chain keto acid hydrazone derivatives: optimization of techniques and application to branched-chain keto acid balance studies across the forearm.

A sensitive method of quantifying branched-chain keto acids in plasma and whole blood samples is described. It is based on the separation by ion-pair reversed-phase liquid chromatography of 2,4-dinitrophenylhydrazine derivatives with ultraviolet detection. The sample clean-up steps that are usually required for reversed-phase high-performance liquid chromatography are eliminated. A reduction in ketoisocaproate isomer formation is obtained by incubation of derivatives in ice. The method is reproducible (coefficient of variation 2%, n = 5, at the 200-pmol level) and the ultraviolet response is linearly related to branched-chain keto acid concentration. Recoveries are high (greater than 95%). Other keto acids do not co-elute with branched-chain keto acids. Because of its sensitivity and precision, this method can be proposed for whole blood branched-chain keto acid balance studies across organs.

Biological Transport↗
PubMed1991

Renal ammoniagenesis in humans with chronic potassium depletion.

Renal ammonia production and distribution and ammonia precursor utilization were evaluated in eight patients with chronic potassium depletion (CPD) and aldosterone-producing adenoma and in 20 controls. In CPD, urinary ammonia excretion and ammonia added to renal venous blood were about twofold higher than in controls; thus, total ammonia production was significantly augmented (88.0 +/- 10.3 mumol/min.1.73 m2 vs. 45.0 +/- 2.6 in controls). Total ammonia production was inversely correlated with serum potassium and directly correlated with urine flow. Stepwise multiple regression analysis showed that both factors, mainly serum potassium, significantly influence ammonia production and account for 61.4% of variations in ammonia production. Renal extraction of glutamine was significantly increased (56.6 +/- 5.9 mumol/min.1.73 m2 vs. 34.6 +/- 3.1 in controls), and this could account for ammonia production. The ratio of urinary ammonia excretion to total ammonia production, an index of the intrarenal ammonia distribution, was similar in patients and controls, and was significantly correlated with urine pH and true renal blood flow (RBF). Stepwise multiple regression analysis showed that RBF, urine pH and urine flow also significantly affected ammonia distribution. However, these factors accounted for only 41.7% of variations in intrarenal ammonia partition, urine pH having a minor role. We conclude that in patients with CPD other factors besides urine pH, urine flow and RBF intervene in the ammonia partition between urine and blood.

Acid-Base Equilibrium↗