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- Ljungdahl, M, et al.
(författare)
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Bacterial translocation in experimental shock is dependent on the strains in the intestinal flora.
- 2000
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 35, s. 389-
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Enteric microorganisms are responsible for a significant proportion of post-surgical infections. Intestinal mucosal injury may permit translocation of bacteria and endotoxin. This study investigates translocation in peritonitis and ischemia/reperfusion by inoculating different bacterial species into the small intestine.METHODS: Twenty-five pigs were monitored hemodynamically and divided into three groups: controls (C), ischemia/reperfusion (I/R), and peritonitis (P). Intramucosal pH (pHi) was calculated tonometrically. A perfusion tube was positioned in the ileum for inoculation of the bacterial strains. In a first study period a non-pathogenic bacterium was used, whereas Escherichia coli strains with known ability to translocate were used in a second. Blood and mesenteric lymph nodes (MLNs) were obtained for bacterial culture and endotoxin analyses.RESULTS: Mesenteric arterial blood flow and pHi decreased in groups I/R and P. Endotoxin levels increased in these groups in period 1, whereas in period 2 an increase over time was only observed in group P. No bacterial translocation to blood or MLNs occurred in period 1. In period 2 bacteria translocated to MLNs in all animals, including controls. Translocation to central and/or mesenteric venous blood was found in all groups, but mainly in I/R and P. The incidence of mucosal injury was similar in the two periods.CONCLUSIONS: Since positive blood and MLN samples were only found in period 2, we conclude that translocation of bacteria seems to be more dependent on the presence of translocating strains in the intestinal bacterial flora than on the mucosal insult.
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- Ljungdahl, M, et al.
(författare)
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Intestinal blood flow and intramucosal pH in experimental peritonitis.
- 1999
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322 .- 1540-0514. ; 11:1, s. 44-50
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: Experimental peritonitis causes gut intramucosal acidosis indicating intramucosal ischemia. However, tissue acidosis may reflect other conditions than ischemia. An increased mucosal-arterial Pco2 difference ( Pco2-gap) is suggested to be a more adequate measure of tissue ischemia than intramucosal pH (pHi). This study was performed to elucidate whether keeping cardiac index (CI) and splanchnic blood flow normal or supranormal by administration of colloids and an inotropic drug could prevent the acidosis as well as reduce the Pco2-gap. A secondary aim was to study to what degree the low pHi in peritonitis really reflects ischemia.SUBJECTS: 24 anesthetized pigs (18-27 kg) divided into four groups.MODELS: A Swan-Ganz catheter, transonic flow meters and catheters for blood sampling were applied. pHi was calculated using tonometry. Standardized fecal peritonitis was induced, except in controls. One peritonitis group was given dextran (Group P(DEX)) and another in addition dobutamine (Group PDOB) to keep CI normal or supranormal, respectively.RESULTS: After 4 h, a significant drop in pHi was found in all peritonitis groups, most pronounced in untreated peritonitis (to 7.09+/-.02). Corresponding values in Group P(DEX) and Group P(DOB) were 7.22+/-.03 and 7.22+/-.01, respectively, and in controls 7.30+/-.02. The Pco2-gap and the mucosal-arterial [H+] difference ([H+]-gap) increased significantly in untreated peritonitis but did not increase in groups given dextran and dextran + dobutamine.CONCLUSION: Maintaining CI in peritonitis attenuated the reduction in pHi and prevented the increased Pco2- and [H+]-gap. It seems justified from these data to conclude that the somewhat reduced pHi in treated peritonitis groups did not reflect tissue ischemia.
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- Ljungdahl, M, et al.
(författare)
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Intramucosal pH and pCO(2) do not strictly correlate with intestinal energy metabolism in experimental peritonitis.
- 2000
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Ingår i: European Surgical Research. - : S. Karger AG. - 0014-312X .- 1421-9921. ; 32:3, s. 182-90
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Tidskriftsartikel (refereegranskat)abstract
- This study aimed to investigate tissue hypoxia on the cellular level in sepsis. Eighteen pigs weighing 18-27 kg were studied. Intramucosal-arterial PCO(2) gradient (PCO(2)-gap) and intramucosal pH (pH(i)) were calculated using tonometry. A blind loop of the small intestine was constructed for repeated tissue biopsies to measure intestinal energy-related metabolites and lactate concentration. Six animals served as controls. In 12 animals, faecal peritonitis was induced. Six of these animals were studied without further interventions, while the others were resuscitated with dextran to maintain cardiac index at baseline level. Untreated peritonitis caused an increase in PCO(2)-gap and a drop in pH(i). The intestinal energy metabolism was not disturbed until the end of the experimental period, with a decreased energy charge value and a moderately increased lactate concentration. In peritonitis-dextran animals, PCO(2)-gap and pH(i) remained at baseline level and the energy metabolism was not disturbed. We conclude that in peritonitis, PCO(2)-gap - like pH(i) - can be influenced by other factors than strictly anaerobic tissue metabolism.
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- Ljungdahl, M, et al.
(författare)
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Small intestinal mucosal pH and lactate production during experimental ischemia-reperfusion and fecal peritonitis in pigs.
- 1997
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322 .- 1540-0514. ; 7:2, s. 131-8
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to investigate mucosal pH and lactate production in a porcine model of ischemia/reperfusion and sepsis using both tonometry and a technique for segmental intestinal perfusion. Eighteen pigs (17-23 kg) were anesthetized and mechanically ventilated. They were divided into three groups and followed for 4 h. Group C (n = 6) served as controls. In the ischemia/reperfusion group (I/R; n = 6), the superior mesenteric artery was totally occluded for 60 min. In group P (n = 6), sepsis was induced by fecal peritonitis. Cardiac index (CI) was determined by thermodilution and blood flow in the superior mesenteric artery (QSMA), using a Transonic flow probe. Intramucosal pH (pHi) was calculated using tonometry. A special balloon tube for segmental perfusion was introduced in the midileum for lactate measurement. Lactate and oxygen saturation were measured in arterial blood and in the superior mesenteric vein. CI, QSMA, pHi, and lactate in blood and perfusate remained unchanged in controls. Occlusion of intestinal blood flow induced a fall in pHi from 7.28 +/- .02 to 6.76 +/- .04, a marked rise in lactate in the perfusate, and an increased arteriovenous lactate difference. During reperfusion, pHi tended to return to baseline values. Lactate in the perfusate and the arteriovenous lactate difference decreased. In sepsis there was a continuous reduction in CI and QSMA to 45 +/- 13% and 40 +/- 20% of baseline, respectively. pHi decreased moderately from 7.22 +/- .09 to 6.98 +/- .25. Lactate remained unchanged in blood and perfusate. Microscopic mucosal injury was observed in all animals subjected to ischemia/reperfusion and in three of six pigs in group P. A good association between pHi and lactate production was seen in ischemia/reperfusion. However, in sepsis, lactate in superior mesenteric venous blood or in intestinal perfusate did not increase, despite the fall in pHi. The mechanism causing ischemic mucosal injury has different characteristics in sepsis and in ischemia caused by arterial occlusion.
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