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Biomedical subjects

A Guariglia

Publications and source records attributed to A Guariglia.

At least 37 records · Page 2Linked to original sources
PubMed1987

Skeletal muscle energetics, acid-base equilibrium and lactate metabolism in patients with severe hypercapnia and hypoxemia.

Quadriceps femoris muscle needle biopsies were performed in ten patients with chronic obstructive pulmonary disease and acute respiratory failure and in ten age- and sex-matched healthy control subjects. The main indices of skeletal muscle cell energy metabolism, intracellular acid-base equilibrium and lactate metabolism were evaluated. Reduced ATP and phosphocreatine content, intracellular acidosis related to hypercapnia, increased muscle lactate without alterations of the muscle lactate concentration gradient were observed in the skeletal muscle of the hypercapnic-hypoxemic COPD patients studied, in which group no correlation was found between hypoxia and energy or lactate metabolism parameters. These results suggest that an overall derangement of cell energy metabolism and acid-base equilibrium is present in severely hypercapnic-hypoxemic chronic obstructive pulmonary disease and that in this condition skeletal muscle seems to metabolize anaerobically-even though, in addition to hypoxia, other factors interfering with both cell energy and lactate metabolism are likely to be present.

Acid-Base Equilibrium↗
PubMed1986

Muscle energy metabolism in uremia.

Energy-rich phosphagens were measured in 11 patients with end-stage chronic renal failure and 11 nonuremic subjects. A significant decrease of ATP, phosphocreatine, total adenine nucleotides, lactate, and energy charge was found. The present results can be referred both to glycolytic sequence disturbances and to the lack of substrates characteristic of uremia.

Adenine Nucleotides↗
PubMed1986

Intracellular acid-base and electrolyte metabolism in skeletal muscle of patients with chronic obstructive lung disease and acute respiratory failure.

Quadriceps femoris muscle needle biopsies were performed in 21 patients with chronic obstructive lung disease (COLD) and acute respiratory failure (ARF) and in 21 age-matched healthy control subjects. Muscle samples were analysed to obtain intracellular bicarbonate and pH values from total acid-labile carbon dioxide content. Muscle potassium, magnesium and sodium content were also determined, as well as water compartments. Skeletal muscle of COLD patients with ARF showed intracellular acidosis and reduced potassium and magnesium content. Total muscle water increase was linked to extracellular water increment. It was concluded that in COLD patients with ARF an overall derangement of skeletal muscle metabolism is present.

Acid-Base Equilibrium↗
PubMed1986

Uremic acidosis and intracellular buffering.

Skeletal muscle biopsies were performed in 16 controls and 15 non-dialysed end-stage chronic renal failure (CRF) patients presenting untreated metabolic acidosis. Intracellular bicarbonate, pH, water compartments and electrolytes were determined. In 8 of 15 patients muscle ATP and lactate were measured. Intracellular bicarbonate (HCO3i) and pH (pHi) were obtained by means of muscle total carbon dioxide method: a significant (p less than 0.001) reduction in both intracellular acid--base indexes was found in all patients (pHi 6.82 +/- 13 vs. 7.04 +/- 0.05; HCO3i 6.28 +/- 2.07 vs. 11.86 +/- 0.87). Total muscle as well as extracellular water was increased. Muscle sodium and chloride contents were also increased, while no change in potassium and magnesium was detected. A significant decrease of both muscle ATP and lactate was found. The data lead to the conclusion that chronic retention of acids in CRF results in a depletion of the muscle buffer pool and consequently in intracellular acidosis: the latter could be the main cause of the cell energy metabolism derangement described in uremia.

Acidosis↗
PubMed1986

Effects of low flux-low pressure cardiopulmonary bypass on intracellular acid-base and water metabolism.

In eight patients undergoing open heart surgery for elective myocardial revascularization, extra-intracellular acid-base and water metabolism parameters were studied before and after cardiopulmonary bypass procedures. All patients presented a different degree of metabolic acidosis related to plasma lactate increase. Intracellular acid-base indexes did not change significantly, though all but one patient showed an intracellular buffers consumption. Both total muscle and extracellular water increased, while intracellular water did not change. It was concluded that low flux-low pressure perfusion CPB was related to a substantial preservation of cell integrity.

Acidosis↗
PubMed1985

Intracellular bicarbonate and pH of skeletal muscle in chronic renal failure.

In 11 controls and 10 patients suffering from untreated uraemic acidosis intracellular bicarbonate and skeletal muscle pH (needle biopsy) were determined. In all patients a significant intracellular acidosis, not related to any extracellular indices was found. It is concluded that the chronic proton load is able to effect intracellular buffer composition; moreover the action of other factors such as derangements of cell metabolism and nutritional imbalance could be operating.

Acidosis↗
PubMed1983

[Measurement of intracellular bicarbonate and pH: preliminary study using potentiometric determination of muscle acid-labile CO2].

A method is described for the determination of total acid-labile CO2 (TCO2) and intracellular bicarbonate concentration [HCO3-] in skeletal muscle samples. Surgical biopsies obtained from the quadriceps femoris muscle of 24 Wistar male rats were analyzed for acid-labile CO2 and extra and intracellular water, extracellular water was estimated from the muscle chloride content. TCO2 method utilizes a single diffusion step with absorption of extracted CO2 by sulphuric acid into barium hydroxide and subsequent potentiometric determination of muscle CO2 content. The measured total CO2 content in muscle was 12.01 +/- 1.06 mMol/Kg wet weight when the sample weight was kept in terms of 22-110 mg, assuming a normal membrane potential and a muscle pCO2 equal to femoral vein blood pCO2, calculated intracellular bicarbonate concentration was 12.58 +/- 1.08 mEq/1 H2O i.c. (X +/- D.S.) and intracellular pH was 7.03 +/- 0.04 (X +/- D.S.).

Animals↗
PubMed1978

Studies on bicarbonate reabsorption in chronic renal failure.

The role of nephron loss, extracellular fluid volume (ECFV) expansion and body potassium stores on bicarbonate reabsorption in chronic renal failure (CRF) was evaluated. In 17 CRF and 3 control subjects, tubular HCO3 reabsorption was studied by HCO3 1M titration technique; ECFV (22Na space at 4th hour) and cell K content (muscle biopsy) were also determined. Nephron loss per se does not cause any change of HCO3 reabsorption rate per unit GFR. With ECFV expansion induced by HCO3 infusion, a Tm HCO3 is rapidly reached only in controls and in CRF patients showing a significant basal ECFV expansion. In these subjects reabsorbed HCO3/Na ratio is constant, suggesting that under these conditions, HCO3 reabsorption depends on the same mechanisms that control Na reabsorption. In cell K depleted CRF patients, HCO3 reabsorption rises more than in controls and no Tm HCO3 is detected, at least within the limits of isotonic ECFV expansion induced by titration; in these subjects HCO3 reabsorption does not appear to be limited by natriuretic factors. In CRF subjects with normal ECFV and cell K, there is a greater HCO3 tolerance to ECFV expansion induced by titration technique than in controls.

Absorption↗