ETIOLOGY OF METABOLIC-ACIDOSIS DURING SALINE RESUSCITATION IN ENDOTOXEMIA

We sought to understand the mechanism of metabolic acidosis that resul ts in acute resuscitated endotoxic shock. In six pentobarbital-anesthe tized dogs, shock was induced by Escherichia coli endotoxin infusion ( 1 mg/kg) and was treated with saline infusion to maintain mean arteria l pressure > 80 mmHg. Blood gases and strong ions were measured during control conditions and at 15, 45, 90, and 180 min after endotoxin inf usion. The mean saline requirement was 1833 +/- 523 mL over a 3 h peri od. The total acid load from each source was calculated using the stan dard base deficit. The mean arterial pH decreased from 7.32 to 7.11 (p < .01); pco(2) and lactate were unchanged. Saline accounted for 42% o f the total acid load. However, 52% of the total acid load was unexpla ined. Although serum Na+ did not change, serum Cl- increased (127.7 +/ - 5.1 mmol/L vs. 137.0 +/- 6.1 mmol/L; p = .016). We conclude that sal ine resuscitation alone accounts for more than one-third of the acidos is seen in this canine model of acute endotoxemia, whereas lactate acc ounts for less than 10%. A large amount of the acid load can be attrib uted to differential Na+ and Cl- shifts from extravascular to vascular spaces.