II. The Protective Effect of Intraluminal Glucose as Energy Substrate

Chiu, Chu-Jeng; Scott, H. J.; Gurd, Fraser N.

doi:10.1001/archsurg.1970.01340280036010

Cited by 104 publications

(68 citation statements)

References 6 publications

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“…The unprotected intestinal tissue is exposed to intra-intestinal proteases leading to further damage of villi and submucosal tissue [24]. Intraluminal washout provides protection and minimizes the morphological damage to the intestine after ischemia and reperfusion [25]. In light of the evidence that ischemia-induced gut damage and the formation of activating factors within the intestinal wall are reduced by intra-intestinal pancreatic protease inhibition, it is possible that pancreatic protease-induced disruption of intestinal cells [4]or extracellular matrix proteins [26]may be involved in the pathophysiological generation of inflammatory mediators.…”

Section: Discussionmentioning

confidence: 99%

Pancreatic Protease Inhibition during Shock Attenuates Cell Activation and Peripheral Inflammation

Fitzal

DeLano²,

Young³

et al. 2002

J Vasc Res

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Intestinal ischemia contributes to shock-induced multiple organ failure. Our recent evidence suggests that pancreatic proteases may be involved in the formation of inflammatory activators within an ischemic intestine. These inflammatory mediators are released early into the circulation and may contribute to the severe systemic inflammatory response syndrome (SIRS) during shock. We examined the impact of intra-intestinal pancreatic protease inhibition on acute intestinal ischemia-induced hypotension, the formation of activating factors for cardiovascular cells, as well as cremaster muscle cell death and intestinal injury by intravital microscopy. Male Wistar rats were divided into four groups: (1) a sham group; and experimental groups with 100 min of superior mesenteric artery occlusion (2) without (SMAO group), and (3) with intestinal lavage using Krebs-Henseleit solution (LAV group), or (4) lavage using the protease inhibitor gabexate mesilate in Krebs-Henseleit solution (FOY group, 0.37 mM). Intestinal ischemia and reperfusion-induced hypotension upon reperfusion was accompanied by a significant increase in the level of neutrophil-activating factors in the intestine and plasma. During reperfusion, a significant increase in leukocyte-endothelium interactions in postcapillary venules and parenchymal cell death were observed in the cremaster muscle in LAV and SMAO animals suggesting peripheral neutrophil cell activation. Intra-intestinal pancreatic protease inhibition resulted in a stable blood pressure throughout the experiment. Cell activation, leukocyte-endothelial interactions and cell death in the cremaster muscle were almost completely abolished in the FOY group. In addition, ischemia-induced intestinal mucosal injury was attenuated with intestinal pancreatic protease inhibition. These results indicate that intestinal pancreatic protease inhibition significantly attenuates intestinal ischemia-induced shock by reducing SIRS and gut injury.

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Section: Discussionmentioning

confidence: 99%

Pancreatic Protease Inhibition during Shock Attenuates Cell Activation and Peripheral Inflammation

Fitzal

DeLano²,

Young³

et al. 2002

J Vasc Res

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“…The pathology score was assessed based on a procedure modified from Chiu (57,58), which included a direct inspection of all microvilli over a 4-cm stretch of jejunum as described (27).…”

Section: Histopathology and Immunohistochemistry Analysismentioning

confidence: 99%

Activation of the Lectin Pathway by Natural IgM in a Model of Ischemia/Reperfusion Injury

Zhang

Takahashi

Alicot

et al. 2006

The Journal of Immunology

129

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Reperfusion of ischemic tissues elicits an acute inflammatory response involving serum complement, which is activated by circulating natural IgM specific to self-Ags exposed by ischemia. Recent reports demonstrating a role for the lectin pathway raise a question regarding the initial events in complement activation. To dissect the individual roles of natural IgM and lectin in activation of complement, mice bearing genetic deficiency in early complement, IgM, or mannan-binding lectin were characterized in a mesenteric model of ischemia reperfusion injury. The results reveal that IgM binds initially to ischemic Ag providing a binding site for mannan-binding lectin which subsequently leads to activation of complement and injury.

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“…Certain authors (2,5) have claimed that the intraluminal glucose alone, acting as an energy supply for the ischaemic mucosa, is responsible for this protective effect. However the results of BOUNOUS (I), implying an influence of endogenous trypsin in aggravating the effects of the ischaemia, would rather suggest that the simple fact of washing the intestine would protect the epithelium.…”

mentioning

confidence: 99%

Protection of the intestinal mucosa during ischaemia by intraluminal perfusion

1975

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The function of the intestinal mucosa immediately after one hour's ischaemia was examined by means of tests in vivo and in vitro. During the ischaemia, the intestinal loop was perfused with media of different compositions, in an attempt to assess which provided the best protection of the epithelium from the deleterious effects of the ischaemia. The absorption of water, ions and glucose was then monitored in vivo, and the uptake of phenylalanine and beta methyl-glucoside by slices of mucosa was determined in vitro. The unprotected mucosa loses all active transport capacity in vitro following one hour's ischaemia, and is the site of a pronounced loss of water and ions into the lumen in vivo. Glucose absorption in vivo is also abolished. If the loop is perfused during the ischaemia with glucose-containing Krebs bicarbonate buffer, much of the transport capacity in vitro is retained; the loss of ions and water is prevented, and glucose absorption in vivo occurs. Perfusion during the ischaemia with other media, such as isotonic mannitol, Krebs bicarbonate buffer, or Ringer-lactate solution, results in a marked protection of the mucosa, in comparison with the unperfused loop, but the effects are not as pronounced as those of the glucose-containing buffer. It is concluded that the act of perfusing the intestine is the most beneficial factor, but that the presence of glucose in the perfusate does afford added protection.

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II. The Protective Effect of Intraluminal Glucose as Energy Substrate

Cited by 104 publications

References 6 publications

Pancreatic Protease Inhibition during Shock Attenuates Cell Activation and Peripheral Inflammation

Pancreatic Protease Inhibition during Shock Attenuates Cell Activation and Peripheral Inflammation

Activation of the Lectin Pathway by Natural IgM in a Model of Ischemia/Reperfusion Injury

Protection of the intestinal mucosa during ischaemia by intraluminal perfusion

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