| 1. |
- Rasmussen, I, et al.
(författare)
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Detection of liver ischemia using microdialysis during experimental peritonitis in pigs.
- 1994
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322 .- 1540-0514. ; 1:1, s. 60-6
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Tidskriftsartikel (refereegranskat)abstract
- The liver oxygen delivery (DO2) and consumption (VO2) were measured in a porcine model of septic shock induced by fecal peritonitis. Lactate and hypoxanthine were simultaneously monitored in hepatic extracellular fluid and in central venous blood using a microdialysis technique. Animals were divided into a control group (n = 6) and a peritonitis group (n = 6). Peritonitis was induced by installation of a standardized amount of autologous feces into the abdominal cavity. The animals were followed for 5 h. The changes in the liver during peritonitis were, a decreased DO2, a increased, maintained, or decreased VO2, an increased oxygen extraction, and a loss of net hepatic lactate uptake. Parallel to these changes, systemic lactic acidosis developed. Intrahepatic lactate and hypoxanthine increased during peritonitis reflecting liver ischemia. The increase of these metabolites was seen concomitantly in the liver and in central venous blood. There was a wide variability of the individual response to the septic challenge among the animals. The limited hepatic oxygen delivery, and the increased needs for oxygen led to flow-dependent oxygen consumption, and signs of liver ischemia in severe sepsis. Intrahepatic and intravenous microdialysis may be useful for monitoring of the individual time course of hepatic and systemic ischemia in sepsis.
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| 2. |
- Arvidsson, D, et al.
(författare)
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Splanchnic oxygen consumption in septic and hemorrhagic shock.
- 1991
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Ingår i: Surgery. - 0039-6060 .- 1532-7361. ; 109:2, s. 190-7
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Tidskriftsartikel (refereegranskat)abstract
- Oxygen consumption (VO2) is dependent on oxygen delivery (DO2) in septic shock. Local hypoxia with later secondary organ failure may develop, however, despite an often hyperdynamic circulation. The splanchnic organs seem to be of vital importance in this context. In experiments performed in pigs we compared total body VO2 and DO2 with oxygen consumption and delivery in the gastrointestinal organs and the liver in two different shock states: (1) septic shock induced by peritonitis (n = 6) and (2) hemorrhagic shock (n = 6). Another group of six animals not in shock served as controls. Total, gastrointestinal, and liver DO2 decreased in a similar pattern in both septic and hemorrhagic shock. Gastrointestinal and liver VO2 increased in sepsis, whereas it was unchanged in hemorrhage. In the later phase of sepsis, liver VO2, but not gastrointestinal VO2, again decreased, because liver oxygen extraction was almost total and liver DO2 decreased further. The development of flow-dependent liver hypoxia was reflected in a decrease in liver lactate turnover (increased liver lactate release) during late sepsis. Early hypoxia in the splanchnic region is suggested as a plausible mechanism behind the development of secondary organ failure, especially in sepsis.
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| 3. |
- Farzad, A, et al.
(författare)
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Luminal release of hyaluronan (hyaluronic acid) in intestinal ischemia in the rat.
- 1993
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Ingår i: Digestion. - 0012-2823 .- 1421-9867. ; 54:3, s. 168-72
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Tidskriftsartikel (refereegranskat)abstract
- Hyaluronan (HA) is a glycosaminoglycan, the water-binding properties of which are suggested to be pivotal for an optimal hydration of tissues. The lamina propria of the intestinal villi is characterized by a high concentration of HA. Increased amounts of HA are observed in the intestinal lumen in patients with Crohn's disease. We have evaluated whether epithelial denudation as such is sufficient to increase the concentration of HA in the lumen of the small intestine. Epithelial damage was accomplished by reversible ischemia-reperfusion injury to the rat ileum and the concentration of HA was determined in luminal perfusate. The perfusate concentration of HA was increased from 26 +/- 8 micrograms/l before ischemia, to 68 +/- 13 and 41 +/- 12 micrograms/l 0-30 and 30-60 min after a 60-min period of subtotal ischemia without venous stasis (p < 0.05). In sham-operated animals, in contrast, the perfusate concentration of HA was virtually unchanged (31 +/- 18, 13 +/- 3 and 10 +/- 1 microgram/l, respectively). Specific staining for HA on sections revealed loss of HA from the villus tips after ischemia. The results show that epithelial denudation results in loss of HA from the villus interstitium to the intestinal lumen.
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| 4. |
- Haglund, U, et al.
(författare)
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Oxygen-free radicals (OFR) and circulatory shock.
- 1991
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Ingår i: Circulatory shock. - 0092-6213. ; 34:4, s. 405-11
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Tidskriftsartikel (refereegranskat)abstract
- During the past decade a large body of information has been collected showing that formation of short-lived highly reactive metabolites (i.e., radicals) constitutes an important principle of tissue injury. There are several sources of information which suggest that radicals are formed in connection with tissue ischemia and shock, and they may then cause damage to cells and contribute to the pathophysiology of ischemia and shock. In the present review we attempt to discuss how radicals damage tissue as well as the data which suggest that radicals are causing tissue injury in shock.
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| 5. |
- Haglund, U, et al.
(författare)
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Oxygenation of the gut mucosa.
- 1993
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Ingår i: British Journal of Surgery. - : Oxford University Press (OUP). - 0007-1323 .- 1365-2168. ; 80:8, s. 955-6
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Tidskriftsartikel (refereegranskat)
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| 6. |
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| 7. |
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| 8. |
- Rasmussen, I, et al.
(författare)
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Early gut ischemia in experimental fecal peritonitis.
- 1992
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Ingår i: Circulatory shock. - 0092-6213. ; 38:1, s. 22-8
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Tidskriftsartikel (refereegranskat)abstract
- Tissue oxygenation in the gastrointestinal tract was studied in a porcine model in which septic shock was induced by fecal peritonitis. The oxygen delivered was estimated by measuring the portal venous blood flow and the calculated arterial oxygen saturation. The oxygen consumption of the gut, including the pancreas and spleen, was monitored by measuring the portal venous blood flow and the difference between the calculated arterial oxygen and the measured portal venous oxygen saturation. In addition, the oxygenation of the gut mucosa was followed via the tonometric technique. Furthermore, lactate was measured in arterial and portal blood. The experimental animals were divided into two groups, one control (n = 6) and one experimental (n = 6). Peritonitis was introduced by installation of a standardized amount of autologous feces into the abdominal cavity. The animals were followed for 5 hr. Very early during the course of sepsis there was a fall in gut intramucosal pH (pHi), and this was evident before any reduction in splanchnic DO2. Furthermore, an early increase in splanchnic VO2 was evident simultaneously with the fall in pHi. Arterial pH and lactate were not able to detect the inadequate regional tissue oxygenation. It is concluded that pHi measured with the tonometric technique is sensitive in detecting gut mucosal ischemia, and it is therefore highly likely that tonometry would be a valuable method in monitoring severe ill patients.
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| 9. |
- Rasmussen, I, et al.
(författare)
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Hepatic oxygen consumption and cytochrome P450 activity in experimental faecal peritonitis.
- 1993
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Ingår i: European Journal of Surgery. - 1102-4151 .- 1741-9271. ; 159:4, s. 201-7
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To study hepatic oxygen consumption and cytochrome P450 activity in pigs with septic shock induced by faecal peritonitis.DESIGN: Controlled experimental study.ANIMALS: 12 pigs weighing 19-27 kg.INTERVENTION: The animals were divided into a control group (n = 6) and a peritonitis group (n = 6). Peritonitis was induced by intraperitoneal instillation of a standard amount of autologous faeces. The animals were then observed for 300 minutes. Liver biopsy specimens were taken at 0 and 300 minutes.MAIN OUTCOME MEASURES: Hepatic oxygen delivery (DO2) and consumption (VO2). Cytochrome P450 activity was studied by measuring O- and N-demethylation of codeine at 0 and 300 minutes.RESULTS: Hepatic DO2 was reduced, whereas VO2 was increased during sepsis. There were no significant changes in the N- and O-demethylation of codeine.CONCLUSIONS: Hepatic VO2 did increase during sepsis, possibly because of the increased metabolic demand. Cytochrome P450 activity was unaffected by the septic challenge.
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| 10. |
- Rasmussen, I, et al.
(författare)
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Splanchnic and total body oxygen consumption in experimental fecal peritonitis in pigs : effects of dextran and iloprost.
- 1992
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Ingår i: Circulatory shock. - 0092-6213. ; 36:4, s. 299-306
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Tidskriftsartikel (refereegranskat)abstract
- Tissue oxygenation in the gastrointestinal tract and in the liver was studied in a porcine model where septic shock was induced by fecal peritonitis. The effects of different fluid regimes were compared. In one group (n = 8) a moderate amount of crystalloid fluids was given, in another (n = 7) crystalloids and colloids, and in a third group (n = 6) iloprost, a prostacyclin analogue, was administered intra-arterially (10 ng x kg-1 b.w. x min-1) in combination with the crystalline and colloid fluid regime. Septic shock induced by fecal peritonitis reduced cardiac index and oxygen supply to splanchnic organs. Iloprost improved the hepatic arterial blood flow, and tended to attenuate the reduction in liver oxygen delivery. Oxygen consumption (VO2) in the gastrointestinal tract and the liver was significantly increased in the group given crystalloids. These animals developed a hypovolemic/hypodynamic septic shock. Liver VO2 in these animals became flow dependent reflected by increasing hepatic venous lactate values and inversion of lactate turnover by the liver. In the two other groups gastrointestinal and liver VO2 remained constant during the observation period. Oxygen extraction over the liver increased when oxygen delivery decreased. The increased liver VO2 is suggested to be secondary to impaired microcirculation and accumulation of macrophages and leukocytes in the septic liver.
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