EFFECTS OF SODIUM-BICARBONATE ON STRIATED-MUSCLE METABOLISM AND INTRACELLULAR PH DURING ENDOTOXIC-SHOCK

The effects of HC03Na load on acid-base balance and muscle intracellul ar bioenergetics have been investigated using P-31-magnetic resonance spectroscopy in an experimental model of endotoxinic shock. Anesthetiz ed, mechanically ventilated, and paralyzed rats (n = 16) were given an intravenous bolus of Escherichia coli lipopolysaccharide (15 mg/kg). When shock was established they were randomly assigned to receive eith er HCO3Na intravenously (2 mmol/kg in 2 min) or an equimolar saline in jection. Lipopolysaccharide induced a significant decrease in the leve ls of mean arterial pressure (58 +/- 6 vs. 120 +/- 8 mmHg), arterial p H (7.20 +/- .03 vs. 7.35 +/- .01), intracellular pH (6.86 +/- .04 vs. 7.08 - .01), a marked hyperlactatemia (7 +/- 3 vs. 1.2 +/- .2 mmol/L) and a drop in the phosphocreatine-inorganic phosphate ratio. In the bi carbonate-loaded rats, mean arterial pressure further decreased wherea s it remained unchanged in the saline group. Bicarbonate increased art erial pH and PaCO2 transiently. In the saline group, arterial pH decre ased and PaCO2 remained stable. In both groups, intracellular pH and h igh energy phosphates had a similar evolution. In this model of septic shock, partial correction of arterial pH using HCO3Na did not reduce the metabolic cellular injury in skeletal muscle. Based on these resul ts, HCO3Na may be of limited therapeutic value in severe septic metabo lic acidosis.