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.

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.

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.

[Measurement of intracellular bicarbonate and pH: preliminary study using potentiometric determination of muscle acid-labile CO2]. / Misurazione del bicarbonato e del pH intracellulari: rilievi preliminari mediante determinazione potenziometrica della CO2 acido-labile muscolare.

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.).