A Report on Associations Among Gastric pH, Bleeding, Duodenogastric Reflux, and Outcomes After Trauma
Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston-Medical School, Houston, Texas, USA. The Journal of trauma
(Impact Factor: 2.96).
01/2008; 64(1):105-10. DOI: 10.1097/TA.0b013e31815ebd99
The pathogenesis of multiple organ failure (MOF) in trauma patients may involve the gastrointestinal tract, but its exact origins remain elusive. In a prospective study, the gastric fluid of major torso trauma patients was examined for evidence of duodenogastric reflux and potential gastric injury, and was compared with patient outcomes regarding MOF.
Patient samples were collected daily for 4 days by nasogastric tube and analyzed for pH, hemoglobin, and bile acid. Blood was collected for analysis of C-reactive protein (CRP). Outcomes were recorded for the presence or absence of MOF.
The results showed that most patients exhibited alkaline gastric contents (pH >/=4.9) and elevated levels of hemoglobin immediately after the trauma. Although non-MOF patients demonstrated a decline of both mean gastric pH and bleeding by day 4, MOF patients maintained significant elevations in pH during this time period. Mean total bile acid levels were increased in all patients, signifying the presence of duodenogastric reflux. However, there were no clear differences in mean bile acid concentrations between MOF and non-MOF patients over time, although MOF patients tended to exhibit higher levels. All patients showed a progressive rise in serum CRP during the first 24 hours after trauma, which was maintained for 4 days. The initial rise in serum CRP in MOF patients was delayed compared with that in non-MOF patients.
We conclude that duodenogastric reflux occurs in trauma patients in the first few days after trauma and may contribute to elevated gastric pH and bleeding. Further study is needed to verify whether monitoring the gastric juice of trauma patients during the first several days of hospitalization, for alkaline pH and excessive blood in the gastric lumen, could lead to better assessments of patient status.
Available from: ncbi.nlm.nih.gov
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ABSTRACT: Endotoxemia from sepsis can injure the gastrointestinal tract through mechanisms that have not been fully elucidated. We have shown that LPS induces an increase in gastric permeability in parallel with the luminal appearance of secretory phospholipase A2 (sPLA2) and its product, lysophosphatidylcholine (lyso-PC). We proposed that sPLA2 acted on the gastric hydrophobic barrier, composed primarily of phosphatidylcholine (PC), to degrade it and produce lyso-PC, an agent that is damaging to the mucosa. In the present study, we have tested whether lyso-PC and/or sPLA2 have direct damaging effects on the hydrophobic barriers of synthetic and mucosal surfaces. Rats were administered LPS (5 mg/kg, i.p.), and gastric contents were collected 5 h later for analysis of sPLA2 and lyso-PC content. Using these measured concentrations, direct effects of sPLA2 and lyso-PC were determined on (a) surface hydrophobicity as detected with an artificial PC surface and with intact gastric mucosa (contact angle analysis) and (b) cell membrane disruption of gastric epithelial cells (AGS). Both lyso-PC and sPLA2 increased significantly in the collected gastric juice of LPS-treated rats. Using similar concentrations to the levels in gastric juice, the contact angle of PC-coated slides declined after incubation with either pancreatic sPLA2 or lyso-PC. Similarly, gastric contact angles seen in control rats were significantly decreased in sPLA2 and lyso-PC-treated rats. In addition, we observed dose-dependent injurious effects of both lyso-PC and sPLA2 in gastric AGS cells. An LPS-induced increase in sPLA2 activity in the gastric lumen and its product, lyso-PC, are capable of directly disrupting the gastric hydrophobic layer and may contribute to gastric barrier disruption and subsequent inflammation.
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Male rats received saline or ketamine (7 mg/kg ip) 1 hour before saline or LPS (20 mg/kg ip) for 5 hours. Thirty minutes before killing, rats received orogastric rhodamine B isothiocyanate-labeled dextran and 5 minutes later fluorescein isothiocyanate-labeled dextran via a duodenal catheter. GI contents were collected for dye, bile acid, and hemoglobin (index of bleeding) determinations.
LPS significantly impaired intestinal transit and increased duodenogastric bile reflux and gastric luminal hemoglobin content. Ketamine improved intestinal transit, prevented LPS-induced bile reflux, and diminished gastric bleeding. In mechanistic studies, ketamine also attenuated LPS-induced upregulation of the proinflammatory genes inducible nitric oxide synthase and cyclo-oxygenase-2 in the stomach but preserved expression of the anti-inflammatory gene heme-oxygenase-1 (Western blot).
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The gastric mucosa is protected in part by a hydrophobic layer of phosphatidylcholine (PC) that overlies the mucus gel on the stomach. Endotoxin treatment (i.e., lipopolysaccharide [LPS]) results in an apparent disruption of this layer, as evidenced by a reduction in surface hydrophobicity and an increase in transmural permeability. The current studies compared PC and lyso-PC levels in mucus and gastric mucosa before and after LPS treatment, and examined potential mechanisms for surface phospholipid changes.
Rats were administered LPS (5 mg//kg, intraperitoneally) and samples were collected after 5 h for analysis of PC and its primary degradant, lyso-PC, in the loosely and firmly adherent mucus layers and the mucosa. The dependence of LPS-induced effects on gastric alkalinization, PC synthetic activity, and intestinal reflux material was assessed.
The gastric contents after LPS, which also contained duodenal reflux material, had greatly increased amounts of PC and lyso-PC. The firmly adherent mucus layer was unchanged. The gastric mucosa after LPS revealed significant reductions of PC levels and no change in lyso-PC content. These phospholipid changes were not caused by alkalinization of the stomach or altered PC synthesis. Prevention of duodenogastric reflux by pylorus ligation blocked the LPS-induced increase in luminal lyso-PC and the reduction in mucosal PC.
LPS appears to induce a release of PC from gastric mucosa into the lumen, along with degradation of PC to lyso-PC, without an effect on PC synthesis. Component(s) of intestinal reflux material appear to be required for these effects. The lowered PC levels in gastric mucosa after LPS may contribute to reduced barrier properties of this tissue.
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