Response of the intestinal mucosa to ischaemia.

Robinson, J. W. L.; Mirkovitch, V.; Winistörfer, B; Saegesser, F

doi:10.1136/gut.22.6.512

Cited by 85 publications

(53 citation statements)

References 48 publications

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“…The basis for the differential sensitivity of intestinal transport functions to ischemia is not immediately apparent, and the mechanism for the activation of secretion in the face of a mucosal energy deficit remains a matter of speculation. In animal models, the appearance of net secretion precedes the development of histologic evidence of intestinal infarction or gross increases in intestinal permeability and is associated with submucosal vascular stasis (1)(2)(3)5). Thus, one cannot explain the massive fluid losses solely by increased filtration of plasma through damaged mucosa (5).…”

Section: Introductionmentioning

confidence: 99%

“…In animal models, the appearance of net secretion precedes the development of histologic evidence of intestinal infarction or gross increases in intestinal permeability and is associated with submucosal vascular stasis (1)(2)(3)5). Thus, one cannot explain the massive fluid losses solely by increased filtration of plasma through damaged mucosa (5). Alternatively, it has been postulated that secretion could be evoked by a substance released locally during ischemia, although the existence of such a secretagogue has never been demonstrated (6,7,9,10).…”

Section: Introductionmentioning

confidence: 99%

“…Curiously, despite the sudden deprivation of oxygen and nutrients, secretion from the intestinal crypts persists and may, in fact, be stimulated (1)(2)(3)(4)(5)(6)(7). Net intestinal absorption is replaced by secretion, resulting in significant intraluminal fluid sequestration and occasionally diarrhea as an initial manifestation (8).…”

Section: Introductionmentioning

confidence: 99%

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Activation of Cl secretion during chemical hypoxia by endogenous release of adenosine in intestinal epithelial monolayers.

Matthews

Tally²,

Smith³

et al. 1995

J. Clin. Invest.

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Intestinal ischemia is characterized by rapid early inhibition of absorptive function and the appearance of net secretion, although why active secretion persists in the setting of a mucosal energy deficit is unknown. The cryptlike epithelial line T84, a well-characterized model of intestinal Cl -secretion, develops a prominent increase in short-circuit current (I,, indicative of active Cl-transport) in response to "hypoxia" induced by metabolic inhibitors. The increased L is associated with the initial decrease in monolayer ATP content. The LC is transient and disappears with progressive energy depletion, although graded degrees of ATP depletion induce a more sustained L response. Chromatographic analysis and secretory bioassays show that the IS response to metabolic inhibitors is related to the endogenous release of adenosine into the extracellular space in quantities sufficient to interact locally with stimulatory adenosine receptors. Unlike its classical role as a metabolic feedback inhibitor, adenosine appears to function as an autocrine "feedforward" activator of active intestinal Cl -secretion. These studies suggest a novel role for adenosine in the conversion of the gut from an absorptive to a secretory organ during ischemic stress, thus contributing to the initial diarrheal manifestations of intestinal ischemia. (J. Clin. Invest. 1995. 96:117-125.)

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Activation of Cl secretion during chemical hypoxia by endogenous release of adenosine in intestinal epithelial monolayers.

Matthews

Tally²,

Smith³

et al. 1995

J. Clin. Invest.

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“…While the sensitivity of the small intestine to warm and cold ischemia has been studied extensively in terms of morphology and biochemistry [8][9][10][11][12], only a few reports have examined the large bowel after warm ischemia [13][14][15][16][17]. The aim of this experiment is to evaluate and compare the susceptibility of the small and large intestine to warm and cold ischemia using the in vitro Ussing chamber technique, biochemistry, and histopathology.…”

Section: Introductionmentioning

confidence: 99%

Effect of Ischemia on the Canine Large Bowel: A Comparison with the Small Intestine

Takeyoshi

Zhang

Nakamura

et al. 1996

Journal of Surgical Research

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Mucosal injury caused by ischemia and reperfusion has been well documented with the small intestine, but little is known about the colon. In the present study, the effect of warm and cold ischemia on the canine colon was studied and compared to that on the small intestine. After in situ flushing, the small intestine and the colon from six beagle dogs were removed and stored for 0.5, 1.5, and 3 hr at 37°C (warm ischemia) or for 1, 6, 12, 24, 36, and 48 hr at 4°C (cold ischemia). Electrophysiology, permeability, biochemistry, and histopathology of the specimens at each ischemic period and after reperfusion in the Ussing chamber were determined. Warm and cold ischemia induced durationdependent suppression of electrophysiology in both organs, but the colonic mucosa retained higher activity of absorptive enterocytes and cryptic cells than the small intestine. Only the colon showed increased permeability of FITC-conjugated Dextran from the mucosal surface to the submucosal layer after prolonged ischemia. Changes in adenine nucleotides and purine catabolites were not markedly different between the organs. Histopathologic abnormalities during ischemia and after reperfusion were more serious with the small intestine than with the colon. Compared to warm ischemia, hypothermia lessened or delayed these morphofunctional derangements in both organs, which became universally worsened after reperfusion. Colonic mucosa receives morphofunctional derangements from ischemia and reperfusion, but the severity of the damage was much less severe in the colon than in the small intestine.

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“…nutrition have undergone successful intestinal transplantation (1)(2). Because the small intestine is notoriously sensitive to ischemia, intestinal recovery and preservation techniques are important factors in successful intestinal transplantation (3). Whereas much is known about mucosal damage and recovery after intestinal warm ischemia, little is known about the effects that cold preservation and transplantat\on have on the mucosa (3-6~.…”

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confidence: 99%

Mucosal damage and recovery of intestine after prolonged preservation and transplantation in dogs

1995

Gastroenterology

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Background. Although much is known about the mucosal damage that occurs after intestinal warm ischemia and reperfusion and its recovery, little is known about the effect of cold preservation and transplantation on the mucosa. We studied the electrophysiological, biochemical, and histological changes of the intestinal mucosa after preservation for 24 hr and subsequent transplantation.Methods. The small intestines from adult mongrel dogs were harvested. The intestines were orthotopically autotransplanted immediately (control group) or after preservation for 24 hr(preservation group). Jejunal and ileal tissues were taken before harvesting, at the end of preservation, 1 hr after reperfusion, and on postoperative days 3,7, 14, and 28. The Ussing chamber method was used to study the electrophysiologic changes. Tissue maltase, diamine oxidase, and ornithine decarboxylase were measured. A histological analysis was also performed.Results. Control group grafts showed no evident deterioration in electrophysiology, biochemistry, or morphology. In contrast, preservation group grafts exhibited electrophysiological and biochemical degradation, complete denudation of the villi, and crypt injury (especially in the ileum) after reperfusion. Electrophysiologic function and the mucosa biochemical marker recovered within 3 days in the jejunum and within 7-14 days in the ileum; however, histological recovery of mucosal injury required 28 days in the jejunum and more than 28 days in the ileum.Conclus-ions. Our study showed that despite severe destruction of mucosal integrity by prolonged preservation and transplantation, the intestinal mucosa has an enormous regenerative capacity. Our study also showed that regeneration was more pronounced in the jejunum than in the ileum.

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Response of the intestinal mucosa to ischaemia.

Cited by 85 publications

References 48 publications

Activation of Cl secretion during chemical hypoxia by endogenous release of adenosine in intestinal epithelial monolayers.

Activation of Cl secretion during chemical hypoxia by endogenous release of adenosine in intestinal epithelial monolayers.

Effect of Ischemia on the Canine Large Bowel: A Comparison with the Small Intestine

Mucosal damage and recovery of intestine after prolonged preservation and transplantation in dogs

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