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- Fröjse, R, et al.
(författare)
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Local metabolic effects of dopexamine on the intestine during mesenteric hypoperfusion.
- 2004
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322 .- 1540-0514. ; 21:3, s. 241-7
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Tidskriftsartikel (refereegranskat)abstract
- This self-controlled experimental study was designed to test the hypothesis that dopexamine, a synthetic catecholamine that activates dopaminergic (DA-1) and beta2-adrenergic receptors, improves oxygenation in the jejunal mucosa during intestinal hypotension. In six normoventilated barbiturate-anesthetized pigs, controlled reductions in superior mesenteric arterial pressure (PSMA) was obtained by an adjustable clamp around the artery. Dopexamine infusions (0.5 and 1.0 microg.kg(-1).min(-1)) were administered at a freely variable PSMA (i.e., with the perivascular clamp fully open) and at a PSMA of 50 mmHg and 30 mmHg. We continuously measured superior mesenteric venous blood flow (QMES; transit-time ultrasonic flowmetry), jejunal mucosal perfusion (laser Doppler flowmetry), and tissue oxygen tension (PO2TISSUE; microoximetry). Jejunal luminal microdialysate of lactate, pyruvate, and glucose were measured every 5 min. Measurements of mucosal PCO2 (air tonometry), together with blood sampling and end-tidal PCO2 measurements, enabled calculations of pHi and PCO2 gap. Dopexamine reduced mesenteric vascular resistance and increased QMES at a PSMA of 50 mmHg and 30 mmHg. At a PSMA of 30 mmHg, dopexamine increased mesenteric oxygen delivery but did not influence mesenteric oxygen uptake or extraction. In this situation, dopexamine had no beneficial effect on jejunal mucosal blood flow. On the contrary, dopexamine increased mesenteric net lactate production and PCO2 gap, whereas PO2TISSUE and pHi decreased. Jejunal luminal microdialysate data demonstrated an increased lactate concentration and a pattern of decreased glucose concentration and increased luminal lactate-pyruvate ratio. These negative metabolic effects of dopexamine should be taken into account in situations of low perfusion pressures.
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| 2. |
- Nettelbladt, Carl-Gustaf, et al.
(författare)
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Orally inoculated Escherichia coli strains colonize the gut and increase bacterial translocation after stress in rats
- 2003
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Ingår i: Shock. - Philadelphia, USA : Lippincott Williams & Wilkins. - 1073-2322 .- 1540-0514. ; 20:3, s. 251-6
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Tidskriftsartikel (refereegranskat)abstract
- Coliforms are the members of the indigenous gut flora that most often translocate to mesenteric lymph nodes. Very few strains of Escherichia coli found in cecal contents of rats are able to translocate. The present study investigated the role of the composition of the gut flora for the occurrence of bacterial translocation. Two strains of E. coli (KI-C1 and KI-C2), previously shown to translocate in rats subjected to stress, were given by oral inoculation to rats lacking these strains. A biochemical fingerprinting method was used to identify bacteria in cecal contents, on cecal epithelium, and in mesenteric lymph nodes. In a challenge study, the inoculated E. coli strains were shown to colonize the rats and persist for up to 75 days in cecum. Subsequently, one group was starved for 24 h and a second group was subjected to experimental hemorrhage and then starved for 24 h before sampling for bacteriological analyses from blood, cecum, and mesenteric lymph nodes. Two parallel groups of rats served as controls and were not inoculated but otherwise received the same treatment before sampling. In the inoculated group, starved for 24 h, seven out of 11 rats showed translocation, whereas in the noninoculated group one of 11 rats showed translocation (P < 0.05). In groups subjected to hemorrhage and then starved for 24 h, 15/22 rats in the inoculated and 5/20 rats in the noninoculated group showed translocation (P < 0.01). These findings show that orally inoculated KI-C1 and KI-C2 strains can colonize the gut and can substantially increase bacterial translocation in rats subjected to mild and severe stress. The composition of the gut flora seems to be an underestimated factor in the pathophysiology of bacterial translocation.
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| 4. |
- Deng, XM, et al.
(författare)
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The involvement of multiple protease-antiprotease systems and gut origin sepsis in zymosan-associated endothelial barrier injury and multiple organ dysfunction in rats
- 2001
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Ingår i: Shock. - 1540-0514. ; 16:4, s. 298-303
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Tidskriftsartikel (refereegranskat)abstract
- Multiple organ dysfunction syndrome is a dominant cause of mortality in the intensive care unit. Experimentally, a condition similar to the multiple organ dysfunction syndrome can be induced by the intraperitoneal injection of sterile zymosan. In the present study we investigate potential alterations in multiple organ functions, endothelial permeability, and antiproteinases after intraperitoneal injection of zymosan at various doses. Zymosan-induced generalized inflammation lead to endothelial barrier injury in multiple organs/tissues, a decrease in systemic arterial pressure, impaired organ function and gut defence function, and consumption of protease inhibitors, particularly the consumption of alpha (2) antiplasmin. Endothelial barrier injury appears to present a dose- and organ-dependent pattern in multiple organs/tissues, and the increase in endothelial barrier permeability occurred prior to organ dysfunction. Zymosan induced the development of multiple organ dysfunction syndrome, probably initiating multiple protease-antiprotease systems, particularly the fibrinolytic system, leading to endothelial barrier injury, tissue edema, parenchymal cell damage, and eventual organ dysfunction, potentially augmented by a secondary bacterial infection.
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| 6. |
- Holbeck, Staffan, et al.
(författare)
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Hypovolemia is a main factor behind disturbed perfusion and metabolism in the intestine during endotoxemia in cat.
- 2002
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Ingår i: Shock. - 1540-0514. ; 18:4, s. 367-373
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Tidskriftsartikel (refereegranskat)abstract
- Disturbances in intestinal metabolism and perfusion during SIRS can be direct effects of toxic substances, and/or effects secondary to hypovolemia. An attempt to evaluate the significance of hypovolemia for intestinal disturbances during SIRS was made in the present study on feline by evaluating the degree to which the intestinal alterations following endotoxin infusion were restored by a clinically relevant volume infusion. The results were compared with control animals treated identically except that they were not given a volume infusion. We analyzed effects of a colloid infusion during endotoxemia on intestinal perfusion, and on the metabolites lactate, pyruvate, glucose, and glycerol in the intestinal wall, the latter by a microdialysis technique. Arterial and central venous blood pressures, and superior mesenteric artery blood flow were measured, and intestinal oxygen delivery and uptake were calculated. To evaluate to what extent a restoring effect of a colloid infusion was dependent on the type of colloid solution used, three different colloids with about the same volume expanding effects (6% albumin, 6% dextran 70 and 6% hydroxyethyl starch, n = 3 x 6) were tested randomly and blinded. Four hrs after start of endotoxin (1 mg/kg + 1 mg/kg/h), the colloid was infused at a rate of 5 mL/kg for 30 min followed by 2.5 mL/kg/h. Endotoxin caused a marked deterioration of perfusion and metabolic parameters. Most of these parameters turned towards normalization, though not fully reaching baseline values within 4 hrs after start of the colloid infusion. In the control experiments (n = 4), the endotoxin-induced deteriorations persisted or were aggravated during the corresponding time period. The results indicated that hypovolemia is an essential factor but not the only one behind alterations in metabolism and perfusion in the intestine during SIRS, and the alterations can be significantly reduced by adequate volume substitution. In this respect no differences could be seen between the three colloids tested.
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