Increased Plasma D-Lactate is Associated with the Severity of Hemorrhagic/Traumatic Shock in Rats

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.

[1]  J. Gainer,et al.  Trans Sodium Crocetinate for Hemorrhagic Shock: Effect of Time Delay in Initiating Therapy , 2002, Shock.

[2]  John M. Adams,et al.  Trauma-Hemorrhage-Induced Neutrophil Priming Is Prevented by Mesenteric Lymph Duct Ligation , 2002, Shock.

[3]  J. Tenhunen,et al.  LOCAL LACTATE AND HISTAMINE CHANGES IN SMALL BOWEL CIRCULATION MEASURED BY MICRODIALYSIS IN PIG HEMORRHAGIC SHOCK , 2002 .

[4]  H. Bitterman,et al.  Divergent Effects of Oxygen Therapy in Four Models of Uncontrolled Hemorrhagic Shock , 2002, Shock.

[5]  I. Chaudry,et al.  Cyclooxygenase-2-mediated regulation of Kupffer cell interleukin-6 production following trauma-hemorrhage and subsequent sepsis. , 2001, Shock.

[6]  Z. Sheng,et al.  Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats. , 2001, World journal of gastroenterology.

[7]  J. Alexander,et al.  Comparison of translocation of different types of microorganisms from the intestinal tract of burned mice. , 2001, Shock.

[8]  J. Young,et al.  Laparotomy potentiates cytokine release and impairs pulmonary function after hemorrhage and resuscitation in mice. , 2001, The Journal of trauma.

[9]  F. Moore,et al.  POST‐INJURY MULTIPLE ORGAN FAILURE: THE ROLE OF THE GUT , 2001, Shock.

[10]  Da-zhong Xu,et al.  Acute Lung Injury after Hemorrhagic Shock is Dependent on Gut Injury and Sex , 2000, The American surgeon.

[11]  F. Moore.  The role of the gastrointestinal tract in postinjury multiple organ failure. , 1999, American journal of surgery.

[12]  W. Fürst,et al.  Test for Stereospecifity of an Automatedd-Lactate Assay Based on Selective Removal ofl-Lactate☆ , 1999 .

[13]  F. Çağlayan,et al.  Serum D-lactate levels as a predictor of intestinal ischemia-reperfusion injury , 1998, Pediatric Surgery International.

[14]  J. Greve,et al.  D‐lactate as an early marker of intestinal ischaemia after ruptured abdominal aortic aneurysm repair , 1998, The British journal of surgery.

[15]  I. Chaudry,et al.  Severe depression of host immune functions following closed-bone fracture, soft-tissue trauma, and hemorrhagic shock. , 1998, Critical care medicine.

[16]  E. Deitch.  ANIMAL MODELS OF SEPSIS AND SHOCK: A REVIEW AND LESSONS LEARNED , 1998, Shock.

[17]  F. D. Di Padova,et al.  Monoclonal antibody to endotoxin attenuates hemorrhage-induced lung injury and mortality in rats. , 1997, Critical care medicine.

[18]  J. Waymack,et al.  Trauma, shock, and gut translocation. , 1996, New horizons.

[19]  H. Redl,et al.  Pathogenesis of Hemorrhage‐Induced Bacteria/Endotoxin Translocation in Rats Effects of Recombinant Bactericidal/Permeability‐Increasing Protein , 1995, Annals of surgery.

[20]  H. Redl,et al.  Kinetics of Endotoxin and Tumor Necrosis Factor Appearance in Portal and Systemic Circulation After Hemorrhagic Shock in Rats , 1995, Annals of surgery.

[21]  Fink Mp.  Effect of critical illness on microbial translocation and gastrointestinal mucosa permeability. , 1994 .

[22]  M. Murray,et al.  Serum D(-)-lactate levels as an aid to diagnosing acute intestinal ischemia. , 1994, American journal of surgery.

[23]  J. Horton,et al.  BACTERIAL TRANSLOCATION AFTER BURN INJURY: THE CONTRIBUTION OF ISCHEMIA AND PERMEABILITY CHANGES , 1994, Shock.

[24]  I. Chaudry,et al.  EVIDENCE FAVORING THE ROLE OF THE GUT AS A CYTOKINE‐GENERATING ORGAN IN RATS SUBJECTED TO HEMORRHAGIC SHOCK , 1994, Shock.

[25]  M. Murray,et al.  Serum D(-)-lactate levels as a predictor of acute intestinal ischemia in a rat model. , 1993, The Journal of surgical research.

[26]  R. Roumen,et al.  Intestinal permeability after severe trauma and hemorrhagic shock is increased without relation to septic complications. , 1993, Archives of surgery.

[27]  D. Altavilla,et al.  Passive immunization with antibodies against tumor necrosis factor (TNF-alpha) protects from the lethality of splanchnic artery occlusion shock. , 1992, Circulatory shock.

[28]  M. Fink.  Gastrointestinal mucosal injury in experimental models of shock, trauma, and sepsis , 1991, Critical care medicine.

[29]  R. Berg.  Bacterial translocation from the gastrointestinal tract. , 1990, Trends in microbiology.

[30]  T. Ziegler,et al.  Increased intestinal permeability associated with infection in burn patients. , 1988, Archives of surgery.

[31]  R. Eng,et al.  d-Lactic Acid Measurements in the Diagnosis of Bacterial Infections , 1986, The Journal of infectious diseases.

[32]  J. Boyle,et al.  D-Lactic acidosis in children: an unusual metabolic complication of small bowel resection. , 1983, The Journal of pediatrics.

[33]  L. Stolberg,et al.  d-Lactic acidosis due to abnormal gut flora: diagnosis and treatment of two cases. , 1982, The New England journal of medicine.

[34]  S. Sauerland,et al.  A pig hemorrhagic shock model: oxygen debt and metabolic acidemia as indicators of severity. , 2001, Shock.

[35]  W. Fürst,et al.  Test for stereospecifity of an automated Dd-lactate assay based on selective removal of Ll-lactate. , 1999, Analytical biochemistry.

[36]  I. Marzi,et al.  Significance of TNF in hemorrhage-related hemodynamic alterations, organ injury, and mortality in rats. , 1996, The American journal of physiology.

[37]  H. Redl,et al.  Involvement of bacteria/endotoxin translocation in the development of multiple organ failure. , 1996, Current topics in microbiology and immunology.

[38]  M. Fink.  Effect of critical illness on microbial translocation and gastrointestinal mucosa permeability. , 1994, Seminars in respiratory infections.

[39]  H. Redl,et al.  Hypovolemic-Traumatic Shock Models in Baboons , 1993 .

[40]  J. Hamar,et al.  Sequence of morphological alterations in a small intestinal ischaemia/reperfusion model of the anesthetized rat. A light microscopy study. , 1992, International journal of experimental pathology.

[41]  Z. Ba,et al.  Differential alterations in plasma IL-6 and TNF levels after trauma and hemorrhage. , 1991, The American journal of physiology.