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Biomedical subjects

G Garibotto

Publications and source records attributed to G Garibotto.

At least 73 records · Page 4Linked to original sources
PubMed1986

Comparative effects of nonionic (iopamidol) and ionic (sodium and meglumine diatrizoate) contrast media for urography on urinary excretion of water and solutes.

Urinary water and solute excretion before and for 40 minutes after intravenous bolus injection of a nonionic (iopamidol) or an ionic medium (sodium meglumine diatrizoate) have been studied in subjects with normal renal function. Iopamidol produced less urinary losses of water, potassium, sodium, and chloride than did diatrizoate; uric acid excretion was also less enhanced. Surprisingly, both contrast agents produced a comparable increase in urinary pH and bicarbonate excretion. These data show that nonionic agents produce fewer changes in urinary excretion of water and solutes; the less enhanced excretion of uric acid after a nonionic medium may be an important reason to choose the latter agents for urography in patients at risk for urate neophropathy.

Bicarbonates↗
PubMed1986

Effects of hemodialysis on guanidinopropionic acid metabolism.

Blood levels of guanidinopropionic acid (GPA), a putative uremic toxin, have been evaluated in 5 uremic patients before a dialytic session, at the end of it and during the following 68 h. GPA levels are markedly higher in uremic patients than in controls and are significantly reduced at the end of dialysis even if still higher than in controls. The clearance of GPA is similar to those of urea and creatinine, even if at the end of the dialysis session the percent decrease of GPA is significantly lower than that of urea. During the first 8 h after the end of dialysis GPA levels increase steeply; subsequently, the rate of accumulation of GPA in blood declines markedly remaining constant until the 68th hour. In conclusion GPA is markedly increased in blood of uremic patients and is significantly removed by dialysis. The evaluation of GPA increase per hour after the end of dialysis may provide an estimation of GPA production in uremic patients.

Adult↗
PubMed1985

Leg metabolism of amino acids and ammonia in patients with chronic renal failure.

Leg metabolism of amino acids and ammonia in the postabsorptive state was evaluated in 10 patients with chronic renal failure (CRF) and in 10 patients with normal renal function (controls) by measuring the arterial-femoral venous (A-FV) differences for free amino acids and ammonia. Total amino acid release from the leg and alanine and glutamine release, which accounts for the greatest amount of the total amino acid release, are similar in patients and controls. Total amino acid uptake from the arterial blood and glutamate uptake, which is the amino acid extracted at the highest rate, are comparable in both groups. Taken together these data, in addition to the similarity of A-FV differences for proteolytic markers, namely tyrosine, phenylalanine and histidine, suggest that protein breakdown in peripheral tissues is not increased in patients with CRF. In CRF selective metabolic abnormalities for some amino acids are evident. Whilst only the A-FV differences for valine, leucine and isoleucine are decreased, additional alterations are observed by relating the A-FV difference for each amino acid to that of proteolytic markers. Such a procedure demonstrates that in CRF histidine release relative to that of proteolytic markers is reduced, whereas proline and arginine release is increased. In CRF the reduced release of some amino acids, mainly branched-chain amino acids, by the leg probably affects the pattern of circulating amino acids. Finally, both in patients and in controls a significant uptake of ammonia is observed; the ammonia uptake is related to arterial levels of this metabolite, confirming the role of peripheral tissues in removing ammonia from circulation.

Adult↗
PubMed1983

Neuroanatomical digital image processing in CT-guided stereotactic operations.

In order to utilize computed tomography (CT) for functional neurosurgical procedures, a number of problems must be resolved. One such problem is the development of an appropriate technique for digital processing of neuroanatomical images. Our previous work concerned a numerical reproduction of a well-known stereotactic atlas and its three-dimensional manipulation. In order to efficiently utilize this information with CT images we propose a technique for data reduction that allows the reconstruction of anatomical structures from the atlas. The logic of implementing these data in CT-assisted stereotactic surgery is described.

Brain↗
PubMed1983

Glucose interorgan exchange in chronic renal failure.

The mechanisms responsible for the altered glucose metabolism observed in chronic renal failure (CRF) were investigated in the postabsorptive state. In 11 patients with CRF and in 15 subjects with normal renal function, the hepato-splanchnic (HS), leg, and brain exchanges of glucose were measured; the HS exchange of gluconeogenic amino acids was also evaluated. Patients with CRF had normal glucose levels, whereas insulin levels and the ratio of insulin to glucose were significantly increased in comparison with controls. In CRF, HS glucose output was slightly lower in comparison with controls (0.46 +/- 0.04 vs. 0.57 +/- 0.04 mmoles/min X 1.73 m2 in controls; P less than 0.1). Arterial levels of alanine and glycine and their uptake by the HS bed were similar in both groups, but in CRF HS serine uptake disappeared, mainly as a consequence of a reduction of its fractional extraction. Conversely, a significant proline extraction became evident, primarily depending on the increased arterial levels of this amino acid. The total HS uptake of potential gluconeogenic amino acids was not different in the two groups, and its ratio to glucose output was increased in CRF (28.0 +/- 4.7 vs. 16.0 +/- 1.9 in controls). In CRF, the arterial-femoral venous differences of glucose were significantly reduced (0.11 +/- 0.04 vs. 0.25 +/- 0.04 mmoles/liter in controls), as was the fractional extraction of glucose in the leg. Finally, in CRF both glucose uptake and its fractional extraction by the brain were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1983

Branched-chain amino acid metabolism in chronic renal failure.

Interorgan exchange of branched-chain amino acids (BCAA) in the postabsorptive state was evaluated in 16 patients with chronic renal failure (CRF) and in 20 subjects with normal renal function, by measuring arterial-venous differences of BCAAs across the leg, brain, hepato-splanchnic (HS) bed, and kidney. In CRF, arterial blood levels of valine are significantly reduced, whereas leucine and isoleucine levels are not different from controls; valine and leucine levels are directly related to GFR. In CRF, a significant decrease in the release of valine by the leg is observed; the leucine release tends to be lower; for both these amino acids, leg release is directly related to their arterial levels. Both ratios of valine and leucine release to total amino acid release by the leg are significantly reduced in CRF. Furthermore, in CRF cerebral uptake and fractional extraction of valine and isoleucine are decreased. In normal subjects, valine and leucine are significantly extracted by the HS bed, whereas in CRF the HS uptake of valine and its fractional extraction fall significantly and leucine uptake is unchanged. The kidney releases significant amounts of leucine both in CRF and in controls. In conclusion, in CRF in the postabsorptive state the exchange of BCAAs, mainly valine, is altered rather early at the major sites of production and utilization, and the flux of these amino acids among the organs is decreased. The primary defect is the decreased output by peripheral tissue, which reduces the supply of BCAAs to the brain and HS bed. Regional metabolic disturbances further impair BCAA utilization.

Adult↗
PubMed1982

Renal ammoniagenesis in an early stage of metabolic acidosis in man.

Total renal ammonia production and ammonia precursor utilization were evaluated in patients under normal acid-base balance and in patients with 24-h NH4Cl acidosis by measuring (a) ammonia excreted with urine and that added to renal venous blood, and (b) amino acid exchange across the kidney. In 24-h acidosis not only urinary ammonia excretion is increased, but also total ammonia production is augmented (P less than 0.005) in comparison with controls. By evaluating the individual role of acid-base parameters, urine pH and urine flow in influencing renal ammonia production, it was shown that the degree of acidosis and urine flow are likely major factors stimulating ammoniagenesis. Both urine pH and urine flow are determinant in the preferential shift of ammonia into urine. In 1-d acidosis, renal extraction of glutamine was not increased and the total ammonia produced/glutamine N extracted ratio was higher than in controls (P less than 0.005) and was inversely correlated with the log of arterial bicarbonate concentration (P less than 0.001). In the same condition, renal glycine and ornithine uptake took place; the more severe the acidosis, the greater was the renal extraction of these amino acids (P less than 0.001). These data indicate that at the early stages of metabolic acidosis, in spite of a brisk increase in ammonia production, the mechanisms responsible for the increased glutamine use, which are operative in chronic acidosis, are not activated and other ammonia precursors, besides glutamine, are probably used for ammonia production.

Acidosis↗
PubMed1981

[Activity of renal enzymes producing ammonia from glutamine in the absence of phosphate in the rat: 1. Effect of chronic metabolic acidosis].

Phosphate- independent glutaminase (PIG) and gamma-glutamyl transpeptidase (gamma GT) activities were evaluated in renal cortex homogenates of rats under normal acid-base balance or chronic metabolic acidosis (CMA). An incubation medium containing glutamine 2 mM, no phosphate, pH 7,40, was used. PIG activity was measured as glutamate production and total gamma GT activity as ammonia production. In normal rats gamma GT activity was significantly higher (0,84 +/- 0,05 mumol/min/g wet wt.) than PIG activity (0,48 +/- 0,06 mumol/min/g wet wt.) (p less than 0,01). In CMA there was a significant increase in PIG activity and an even higher increase in gamma GT activity (p less than 0,01 compared to controls in both cases). The glutamate production/ammonia production ratio was 0,57 +/- 0,05 in normal rats, and 0,37 +/- 0,03 in CMA ( p less than 0,025). These data suggest that the increase in PIG activity and, to a further extent, the increase in gamma GT activity may play an important role in augmenting renal ammonia production in CMA.

Acidosis↗
PubMed1981

[Activity of renal enzymes producing ammonia from glutamine in the absence of phosphate: 2. Effect of phosphate dependent glutaminase inhibition by heating].

UNLABELLED: It is known that heating at 50 degrees C for 10 minutes inhibits phosphate dependent glutaminase (PDG) activity of renal cortex, without any effect on gamma-glutamyl transpeptidase (gamma GT) and its phosphate independent glutaminase (PIG) activity. The effect of heating on PIG and total gamma GT activities was evaluated in renal cortex homogenates of rats both in normal acid-base equilibrium and in chronic metabolic acidosis (CMA). Homogenates were incubated in a medium containing glutamine 2 mM, no phosphate, at pH 7,40. PIG activity was measured as glutamate production and total gamma GT activity as ammonia production. In normal rats PIG activity was unchanged after heating, whereas a significant decrease of total gamma GT activity was observed (p less than 0,01). CMA caused an increase in both PIG and total gamma GT activity (p less than 0,01) and these increased to a further extent after heating. In both normal and acidotic rats the glutamate production/ammonia production ratio rose to about 1. IN CONCLUSION: a) in the experimental setting used for this study PDG activity does not intervene in glutamate and ammonia production from glutamine; b) heating causes an inhibition of gamma GT activities, other than PIG, both in normal and in acidotic rats; c) in CMA heating increases PIG activity of gamma GT.

Ammonia↗
PubMed1980

Amino acid metabolism and the liver in renal failure.

The study of amino acid metabolism across the splanchnic organs can be useful for investigating derangements in nitrogen metabolism in chronic renal insufficiency. For this purpose, arterial-hepatic venous differences for 19 free amino acids, ammonia and urea, determined in whole blood, were measured in six patients with chronic renal insufficiency and in six subjects with normal renal function. In normal conditions, the hepatosplanchnic bed significantly extracts glutamine, alanine, glycine, serine, threonine, lysine, arginine, phenylalanine, valine, tyrosine, histidine, leucine, and ammonia, and releases glutamate, citrulline, and urea. In chronic renal insufficiency, glutamine uptake decreases, serine, valine and ammonia uptake disappears, proline extraction becomes present, citrulline output is no longer detectable and glutamate release falls slightly. Furthermore, the splanchnic uptake of ammonia and the output of urea into the hepatic veins are markedly reduced. Since glutamine and ammonia are major substrates for urea synthesis, their lower uptakes, as observed in renal insufficiency, may be consistent with the reduced urea output. The changes in splanchnic metabolism observed in chronic renal insufficiency have a minor effect on the abnormalities in circulating amino acids. Finally, the splanchnic metabolism shows an important role in the homeostasis of circulating tyrosine and proline.

Adult↗
PubMed1980

Renal metabolism of amino acids and ammonia in subjects with normal renal function and in patients with chronic renal insufficiency.

The net renal metabolism of amino acids and ammonia in the post absorptive state was evaluated in subjects with normal renal function and in patients with chronic renal insufficiency by measuring renal uptake and release, and urinary excretion of free amino acids and ammonia. In normal subjects the kidney extracts glutamine, proline, citrulline, and phenylalanine and releases serine, arginine, taurine, threonine, tyrosine, ornithine, lysine, and perhaps alanine. The renal uptake of amino acids from arterial blood occurs by way of plasma only, whereas approximately a half of amino acid release takes place by way of blood cells. Glycine is taken up from arterial plasma, while similar amounts of this amino acid are released by way of blood cells. In the same subjects total renal ammonia production can be largely accounted for by glutamine extracted. In patients with chronic renal insufficiency (a) the renal uptake of phenylalanine and the release of taurine and ornithine disappear; (b) the uptake of glutamine and proline, and the release of serine and threonine are reduced by 80--90%; (c) the uptake of citrulline and the release of alanine, arginine, tyrosine, and lysine are reduced by 60--70%; (d) no exchange of glycine is detectable either by way of plasma or by way of blood cells; (e) exchange of any other amino acid via blood cells disappears, and (f) total renal ammonia production is reduced and not more than 35% of such production can be accounted for by glutamine extracted, so that alternative precursors must be used. A 140% excess of nitrogen release found in the same patients suggests an intrarenal protein and peptide breakdown, which eventually provides free amino acids for ammonia production.

Adult↗
PubMed1980

Ammonia and amino acid metabolism y the portal-vein-drained viscera in chronic renal insufficiency.

Arterial portal-venous differences (A-PV) of ammonia (NH3) and amino acids (AA) were measured in patients with chronic renal insufficiency (CRI) and in controls. In CRI, NH3 release by the portal-vein-drained viscera (PDV) is not different from controls, Gln uptake decreases, Glu extraction occurs, Pro and Thr output increases and Ser release becomes evident; one third of N released as NH3 and AA can be accounted for by Gln and Glu uptake. The N exchange across the PDV is similar in CRI and in controls.

Adult↗
PubMed1978

Effects of chronic renal insufficiency and metabolic acidosis on glutamine metabolism in man.

1. Arterial concentration and arterial-venous differences of glutamine across the kidney, forearm, hepato-splanchnic bed and brain were measured in patients with chronic renal insufficiency and in patients with normally functioning kidneys before and during chronic ammonium chloride acidosis. 2. In chronic renal insufficiency and in chronic metabolic acidosis there is a rise in glutamine release from the muscles and a suppression of glutamine uptake by the hepato-splanchnic bed and the brain. 3. In chronic renal insufficiency arterial glutamine concentrations is significantly increased in comparison with subjects with normal renal function and either normal acid-base balance or chronic metabolic acidosis. 4. In patients with chronic renal insufficiency the kidney extracts negligible amounts of glutamine, which cannot account for the renal ammonia production measured in the same patients.

Acidosis↗
PubMed1978

Cerebral and hepatic urea synthesis in patients with chronic renal insufficiency.

Urea production by the liver and the brain was evaluated in patients with chronic renal insufficiency and in subjects with normal renal function by measuring the arterial-venous differences of urea across the hepatosplanchnic bed and the brain. In five out of seven patients with chronic renal insufficiency no urea release into the hepatic veins was observed, whereas a high urea output by the brain was measured in 6 out of 8 patients. In the control group urea was released only into the hepatic veins. These data demonstrate a defect in hepatic urea synthesis and a switch to cerebral ureagenesis in chronic renal insufficiency.

Adult↗