Changes in gut intramucosal pH and gut oxygen extraction ratio in a porcine model of peritonitis and hemorrhage

Antonsson, J. B.; Engström, Lennart; Rasmussen, I; Wollert, Staffan; Haglund, Ulf

doi:10.1097/00003246-199511000-00014

Cited by 40 publications

(18 citation statements)

References 20 publications

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“…Theisen et al (39) reported alterations in microvascular blood flow to the gut mucosa in a porcine model of hyperdynamic endotoxic shock (ES). Gut alterations, including ileal mucosal acidosis (3), increase in mucosal permeability (31), and gut ischemia (15), have often been reported after administration of lipopolysaccharide (LPS) or live bacteria. Clinical and laboratory research indicates that gut ischemia may be a pivotal initiating event in the secretion of numerous proinflammatory mediators that causes multiple organ failure (14).…”

mentioning

confidence: 99%

Intestinal preconditioning prevents inflammatory response by modulating heme oxygenase-1 expression in endotoxic shock model

Tamion¹,

Richard²,

Renet³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Gut mucosal injury observed during ischemia-reperfusion is believed to trigger a systemic inflammatory response leading to multiple organ failure. It should be interesting to demonstrate this relationship between gut and multiple organ failure in a sepsis model. Intestinal preconditioning (PC) can be used as a tool to assess the effect of intestinal ischemia in inflammatory response after LPS challenge. The aim of this study was to investigate the protective effect of PC against LPS-induced systemic inflammatory and intestinal heme oxygenase-1 (HO-1) expression. ES was performed with LPS (10 mg/kg iv) with or without PC, which was done before LPS. Rats were first subjected to sham surgery or PC with four cycles of 1 min ischemia and 4 min of reperfusion 24 h before LPS challenge or saline administration. PC significantly reduced fluid requirements, lung edema, intestinal lactate production, and intestinal injury. Inflammatory mRNA expressions for intestine and lung ICAM and TNF were significantly reduced after PC, and these effects were significantly abolished by zinc-protoporphyrin (a specific HO-1 activity inhibitor) and mimicked by bilirubin administration. Intestinal PC selectively increased HO-1 mRNA expression in intestine, but we have observed no expression in lungs. These findings demonstrate that intestinal injury is a important event for inflammatory response and multiple organ injury after LPS challenge. Intestinal HO-1 expression attenuates LPS-induced multiple organ failure by modulating intestine injury and its consequences on inflammatory response. Identification of the exact mechanisms responsible for intestine HO-1 induction may lead to the development of new pharmacological interventions.

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mentioning

confidence: 99%

Intestinal preconditioning prevents inflammatory response by modulating heme oxygenase-1 expression in endotoxic shock model

Tamion¹,

Richard²,

Renet³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Experimental studies have shown that supply-dependent oxygen consumption develops at a pHi of 7·1, and below this level an anaerobic metabolism prevails 14 . Clinical studies have suggested that this threshold is associated with colonic ischaemia and major complications 5,7 -9 .…”

Section: Methodsmentioning

confidence: 99%

Colonic ischaemia and intra-abdominal hypertension following open repair of ruptured abdominal aortic aneurysm

Djavani

Wanhainen

Valtysson

et al. 2009

British Journal of Surgery

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“…[16][17][18][19][20] It has been also shown, by several different techniques, that decreases in blood flow to the gut are paralleled by concordant decreases in pHi and increases in tissue PCO 2 determined by tonometry.…”

Section: The Tonometric Methodsmentioning

confidence: 99%

Gas tonometry for evaluation of gastrointestinal mucosal perfusion: experimental models of trauma, shock and complex surgical maneuvers - Part 1

Figueiredo

Silva

Cruz³

et al. 2002

Acta Cir. Bras.

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Substantial clinical and animal evidences indicate that the mesenteric circulatory bed, particularly the gut mucosa, is highly vulnerable to reductions in oxygen supply and prone to early injury in the course of hemodynamic changes induced by trauma, shock, sepsis and several complex surgical maneuvers. Gut hypoxia or ischemia is one possible contributing factor to gastrointestinal tract barrier dysfunction that may be associated with the development of systemic inflammatory response and multiple organ dysfunction syndrome, a common cause of death after trauma, sepsis or major surgeries. Monitoring gut perfusion during experiments may provide valuable insights over new interventions and therapies highly needed to reduce trauma and sepsis-related morbidity and mortality. We present our experience with gas tonometry as a monitor of the adequacy of gastrointestinal mucosal perfusion in clinical and experimental models of trauma, shock and surgical maneuvers associated with abrupt hemodynamic changes, such as aortic occlusion and hepatic vascular exclusion. Next issue we will be presenting our experience with gas tonometry in experimental and clinical sepsis.

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Changes in gut intramucosal pH and gut oxygen extraction ratio in a porcine model of peritonitis and hemorrhage

Cited by 40 publications

References 20 publications

Intestinal preconditioning prevents inflammatory response by modulating heme oxygenase-1 expression in endotoxic shock model

Intestinal preconditioning prevents inflammatory response by modulating heme oxygenase-1 expression in endotoxic shock model

Colonic ischaemia and intra-abdominal hypertension following open repair of ruptured abdominal aortic aneurysm

Gas tonometry for evaluation of gastrointestinal mucosal perfusion: experimental models of trauma, shock and complex surgical maneuvers - Part 1

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