D-
lactate is produced by indigenous bacteria in the gastrointestinal tract. Mammals do not have the
enzyme systems to metabolize D-
lactate rapidly. The present study was designed to determine the kinetics of circulating D-
lactate levels and to examine whether the severity of
shock affects circulating D-
lactate levels in rats subjected to hemorrhagic/
traumatic shock. Anesthetized rats underwent midline
laparotomy (duration 30 min) and were bled to 30-35 mmHg mean arterial pressure (MAP). After the onset of decompensation, MAP was either increased to 40-45 mmHg immediately by administration of
Ringer's solution (moderate
shock) or after 40% of shed blood volume had been re-infused as
Ringer's solution (severe
shock). MAP was then maintained at 40-45 mmHg for 40 min by further administration of
Ringer's solution (inadequate
resuscitation). Subsequently, adequate
resuscitation was performed for 60 min with shed blood and additional
Ringer's solution.
Metabolic acidosis was significantly more pronounced in severe than in moderate hemorrhagic/
traumatic shock. Plasma D-
lactate levels were already significantly increased at the end of severe hemorrhagic/
traumatic shock and remained high during inadequate
resuscitation. D-
lactate levels were significantly higher after severe than after moderate
shock.
Endotoxin levels did not correlate with
shock severity. Damage to the intestinal mucosa was more profound in severe
shock than in moderate
shock. Our data suggest that hemorrhagic/
traumatic shock is associated with mucosal damage and increased plasma D-
lactate levels. The severity of
shock affects D-
lactate concentrations in plasma. Plasma D-
lactate may be a useful marker of intestinal injury after hemorrhagic/
traumatic shock.