Role of neutrophils in hemorrhagic shock-induced gastric mucosal injury in the rat

Smith, S.Morgan; Holm-Rutili, Lena; Perry, Michael A.; Grisham, Matthew B.; Arfors, Karl-E.; Granger, D. Neil; Kvietys, Peter R.; Russell, Janice

doi:10.1016/0016-5085(87)90907-3

Cited by 154 publications

(46 citation statements)

References 8 publications

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“…Neutrophil adherence to endothelial cells is now considered as an important component of vascular damage within the gastrointestinal microcirculation, including the mucosal injury induced by haemorrhagic shock or ischaemia-reperfusion, as well as that following the administration of PAF, ethanol or non-steroid anti-inflammatory agents (Smith et al, 1987;Hernandez et al, 1987;Granger et al, 1989;Kubes et al, 1990a,b;Kvietys et al, 1990;Wallace et al, 1990;. Adherence of such inflammatory cells to the endothelium, which is promoted by the expression of adhesion molecules on both neutrophils and endothelial cells (see Springer, 1990;Zimmerman et al, 1992 for review), can lead to the local release of cytotoxic mediators, including oxygen radicals (Grisham & Granger, 1988), known to provoke microvascular injury (Parks & Granger, 1983;Parks et al, 1984).…”

Section: Discussionmentioning

confidence: 99%

Time‐dependent enhancement or inhibition of endotoxin‐induced vascular injury in rat intestine by nitric oxide synthase inhibitors

László

Whittle

Moncada

1994

British J Pharmacology

135

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1 The effects of the nitric oxide (NO) synthase inhibitors, N0-nitro-L-arginine methyl ester (L-NAME) and NG-monomethyl-L-arginine (L-NMMA), on the vascular damage induced by the endotoxin, E. coli lipopolysaccharide (LPS), in the ileum and colon were investigated in the conscious rat over a 5 h period. 2 Administration of LPS (3 mg kg-', i.v.) increased ileal and colonic vascular injury after a lag period of 2 h, as determined by the leakage of radiolabelled albumin. 3 Administration of L-NAME (1-5 mg kg-', s.c.) concurrently with LPS, produced a dose-dependent increase in vascular albumin leakage in the intestinal tissues, when determined over a 5 h period. Vascular albumin leakage with LPS and L-NAME (5 mg kg-') was substantially increased after 1 h, reached maximal levels 3 h after administration, and then slowly declined. 4 L-NMMA (50 mg kg-1, s.c.), likewise elevated intestinal albumin leakage when administered concurrently with LPS, but this reached maximal levels after 1 h and rapidly declined over the subsequent 2 h. 5 In control rats, in the absence of LPS challenge, neither L-NAME (5 mg kg-', s.c.) nor L-NMMA (50 mg kg-', s.c.) increased intestinal vascular leakage of albumin over a 5 h period. 6 By contrast, when L-NAME (1-5 mg kg-', s.c.) or L-NMMA (12.5-50mg kg-', s.c.) was injected 3 h after LPS, a dose-dependent reduction in the LPS-provoked vascular albumin leakage was observed. 7 Pretreatment with L-arginine (300 mg kg-', s.c.) 15 min prior to the NO synthase inhibitors, reversed either the potentiation or the inhibition by L-NAME (5 mg kg-', s.c.) or L-NMMA (50 mg kg-', s.c.) of the LPS-induced intestinal vascular damage. 8 These findings indicate that initial suppression of the constitutive NO synthase by L-NAME or L-NMMA following challenge with LPS aggravates the acute vascular injury in the ileum and colon, suggesting a defensive role of NO. By contrast, the delayed administration of NO synthase inhibitors, at a time of known expression of the inducible NO synthase, provides protection against the subsequent damage to the intestinal vasculature.

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Section: Discussionmentioning

confidence: 99%

Time‐dependent enhancement or inhibition of endotoxin‐induced vascular injury in rat intestine by nitric oxide synthase inhibitors

László

Whittle

Moncada

1994

British J Pharmacology

135

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“…In the gastrointestinal tract a role for ROMs has been postulated in various forms of enteritis (1, 2, 15) and gastric ulceration (16,17). Ischemic injury has been the best studied model where ROMs created by an endogenous X/XO reaction and from the respiratory burst of neutrophils seem to be responsible for reperfusion injury, especially through the creation of OH' (18)(19)(20)(21) Prostaglandin release might also be protective to the intestinal mucosa.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport.

Karayalçın

Sturbaum²,

Wachsman³

et al. 1990

J. Clin. Invest.

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The changes in short circuit current (electrogenic a-secretion) of rat colon brought about by xanthine/xanthine oxidase in the Ussing chamber were inhibited by catalase and diethyldithiocarbamate, but not by superoxide dismutase. These results, the reproduction of the response with glucose/glucose oxidase and with exogenous H202, and the lack of effect of preincubation with deferoxamine or thiourea implicate H202, and not 02 or OH, as the important reactive oxygen metabolite altering intestinal electrolyte transport. 1 mM H202 stimulated colonic PGE2 and PGI2 production 8-and 15-fold, respectively, inhibited neutral NaCl absorption, and stimulated biphasic electrogenic a secretion with little effect on enterocyte lactic dehydrogenase release, epithelial conductance, or histology. a-secretion was reduced by cyclooxygenase inhibition. Also, the Cl-secretion, but not the increase in prostaglandin production, was reduced by enteric nervous system blockade with tetrodotoxin, hexamethonium, or atropine. Thus, H202 appears to alter electrolyte transport by releasing prostaglandins that activate the enteric nervous system. The change in short circuit current in response to Iloprost, but not PGE2, was blocked by tetrodotoxin. Therefore, PGI2 may be the mediator of the H202 response. H202 produced in nontoxic concentrations in the inflamed gut could have significant physiologic effects on intestinal water and electrolyte transport. (J.

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“…The other main source of oxygen radicals is the polymorphonuclear leukocyte (PMN), which cell can generate superoxide anions when exposed to appropriate stimuli [10]. Recent studies have demonstrated the involvement of PMN's in the pathogenesis of gastric injury [11] and intestinal ischemia [12]. In this paper, the effects of superoxide dismutase (SOD), a scavenger of superoxide, and/or catalase, a scavenger of hydrogen peroxide, on gastric mucosal injuries induced by water-immersion restraint stress or burn stress were investigated.…”

Section: Discussionmentioning

confidence: 99%

Role of oxygen radicals in the pathogenesis of gastric mucosal lesions induced by water-immersion restraint stress and burn stress in rats.

Yoshikawa

Yoshida

Naito

et al. 1990

J. Clin. Biochem. Nutr.

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SummaryThe formation of gastric mucosal lesions and the increase in thiobarbituric acid (TBA)-reactive substances induced by waterimmersion restraint stress or burn stress in rats were significantly inhibited by the treatment with superoxide dismutase (SOD) and/or catalase. Allopurinol inhibited the formation of gastric mucosal injury induced by burn stress, but not the increase in TBA reactants. A drop in the polymorphonuclear leukocyte (PMN) count induced by an injection of anti-rat PMN antibody did not inhibit the aggravation of gastric mucosal lesions or the increase in TBA reactants in either of the stress models. These results suggest that active oxygen species and lipid peroxidation may play a role in the formation of gastric mucosal damage induced by stress. Reduced microcirculation of the gastric mucosa induced by waterimmersion restraint or burn stress did not change following treatment with SOD and/or catalase, suggesting that the effectiveness of SOD and catalase on the gastric mucosal lesions induced by stress may occur via the scavenging of oxygen radicals, and not through an effect on gastric mucosal microcirculation.

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Role of neutrophils in hemorrhagic shock-induced gastric mucosal injury in the rat

Cited by 154 publications

References 8 publications

Time‐dependent enhancement or inhibition of endotoxin‐induced vascular injury in rat intestine by nitric oxide synthase inhibitors

Time‐dependent enhancement or inhibition of endotoxin‐induced vascular injury in rat intestine by nitric oxide synthase inhibitors

Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport.

Role of oxygen radicals in the pathogenesis of gastric mucosal lesions induced by water-immersion restraint stress and burn stress in rats.

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