Emilio Coffrini

A Preliminary Report on the Effects of Malnutrition on Skeletal Muscle Composition in Chronic Obstructive Pulmonary Disease

Several alterations of electrolyte metabolism have been demonstrated to impair respiratory muscle performance: respiratory muscle function improves after magnesium administration in hypomagnesiemic patients1; an increase in transdiaphragmatic pressure after the correction of hypophosphataemia has been found in hypophosphatemic patients2; low values of maximum inspiratory and expiratory pressure values were significantly increased after phosphate repletion in both hypophosphatemic surgical3 and medical patients.4

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.

CELL METABOLISM RESPONSE TO CARDIOPULMONARY BYPASS IN PATIENTS UNDERGOING AORTO-CORONARY GRAFTING

The main parameters of muscle acid-base, water and energy metabolism were studied in ten patients undergoing low-flux (1.5 l/min/m2), low-pressure (40 to 60 mmHg) hypothermic (26 degrees C) cardiopulmonary bypass (CPB) for aortocoronary grafting; absolute gas exchange and haemodynamic data were also measured throughout the entire CPB period. At the end of CPB a substantial preservation of water and energy metabolic indexes was found; a condition of extracellular metabolic acidosis was apparently sustained by muscle cell anaerobic glycolysis enhancement with a consequent increase of both muscle and plasma lactate content. Subnormal cell phosphocreatine levels as well as reduced bicarbonate buffer stores and decreased intracellular pH, were detected. Direct limiting effects of hypothermia on tissue O2 delivery and muscle oxidative metabolism as well as vasoconstriction and arteriovenous shunting associated with CPB procedures are likely to be involved in the above mentioned alterations of cell metabolism.

Phosphorus Depletion in Limb and Respiratory Muscles of Patients with Chronic Obstructive Pulmonary Disease (COPD): A Preliminary Report

Phosphorus plays a key role in cellular biochemical reactions responsible for energy production, storage, and utilization and represents a major component of membranes and other cell structures: thus, the maintenance of normal phosphorus balance and both normal serum and cellular phosphorus levels is critical for the normal function of the organism.1,2 In both experimental and clinical conditions hypophosphatemia and phosphorus depletion are associated with a wide spectrum of clinical syndromes such as myocardial failure, hepatocellular damage, hemolysis, platelet and leucocyte disfunction, osteomalacia and spontaneous fractures, hypoparathyroidism, impaired glucose tolerance, etc.3 Moreover, neurologic and neuromuscular signs and symptoms such as ataxia, confusion, delirium, tremor, hyporeflexia, skeletal muscle weakness, and rhabdomyolysis have been observed.1,3 Hypophosphatemia and/or phosphorus depletion have been equally indicated as possible determinants of respiratory muscle weakness in the course of respiratory failure.4,5 In fact, an impairment of respiratory muscle contractile properties has been demonstrated in the course of hypophosphatemia, which improves with phosphorus repletion.6,7 Hypophosphatemia is a common finding in the course of respiratory illnesses, with a prevalence of about 25%; in 5% of the same patients serum phosphate (Ps) levels may be extremely low (less than 1 mg% or 0.33 mmol/1).8,9

Intracellular Acid-Base and Energy Metabolism in Uremia: A Preliminary Study on Five Patients Before and During Dialysis Treatment

Failure of uremic patients to excrete end-products of endogenous metabolism necessarily results in a positive acid balance with consequent recruitment of both bone and soft tissue buffers.

Intracellular Acid-Base and Energy Metabolism in Oliguric Acute Renal Failure (OARF)

Acute renal failure is often associated with a condition of metabolic acidosis. However, extracellular acid-base parameters do not seem to be fully representative of the entity of retained acids, since it is the intracellular compartment which is mainly involved in buffering of the acid load (1–2).