Platelet-activating factor: an endogenous mediator of mesenteric ischemia-reperfusion-induced shock

Mózes, T; Braquet, P.; Filep, János G.

doi:10.1152/ajpregu.1989.257.4.r872

Cited by 25 publications

(14 citation statements)

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“…Therefore, circulating neutrophils might be primed and activated either by direct interaction with the vascular endothelium of injured intestine or by inflammatory mediators released from injured local intestine. Oxygen free radicals might be generated by a variety of mediators including xanthine oxidase, 2 phospholipase A 2 , 24 plateletactivating factor, 25 TNF-a, 26 and CINC.…”

Section: Discussionmentioning

confidence: 99%

The role of cytokine-induced neutrophil chemoattractant-1 in neutrophil-mediated remote lung injury after intestinal ischaemia/reperfusion in rats

Ishii¹,

Ishibashi²,

Takayama³

et al. 2000

Respirology

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In the I/R group, the permeability index of the lung, the neutrophil count in pulmonary vascular lavage fluid and bronchoalveolar lavage fluid (BALF), lung myeloperoxidase activity and neutrophil oxidative production were all significantly greater than those in the sham group. Cytokine-induced neutrophil chemoattractant-1 levels in blood and BALF were significantly increased at 240 min after intestinal reperfusion. There was a significant relationship between neutrophils in BALF and CINC-1 level in BALE CONCLUSION: These findings suggest that intestinal reperfusion was associated with activation and accumulation of neutrophils in the lung and resulted in remote lung injury with increased microvascular permeability. Thus, CINC-1 in BALF may induce neutrophil migration from the pulmonary vessels to the interstitium and alveolar spaces in remote lung injury after intestinal I/R.

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Section: Discussionmentioning

confidence: 99%

The role of cytokine-induced neutrophil chemoattractant-1 in neutrophil-mediated remote lung injury after intestinal ischaemia/reperfusion in rats

Ishii¹,

Ishibashi²,

Takayama³

et al. 2000

Respirology

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“…Enhanced plasma levels of endothelin-1 have recently been reported in pathological conditions, including ischaemia (Yasuda et al, 1990;Watanabe et al, 1990) and endotoxin shock (Morel et al, 1989) when enhanced blood PAF levels can also be detected (Doebber et al, 1985;Filep et al, 1989;Montrucchio et al, 1989;M6zes et al, 1989). Since PAF and endothelin-1 exert opposite effects on the vascular tone in most vascular beds (PAF is usually a vasodilator while endothelin-1 is a vasoconstrictor), one might assume that they could modify each other's effects on vascular permeability.…”

Section: Discussionmentioning

confidence: 99%

Effects of endothelin‐1 on vascular permeability in the conscious rat: interactions with platelet‐activating factor

Filep¹,

Sirois

Rousseau

et al. 1991

British J Pharmacology

106

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The objectives of the present experiments were to assess the effects of endothelin‐1 on the macrovascular permeability in selected vascular beds, to study the involvement of platelet‐activating factor (PAF) in vascular responses to endothelin‐1 and to examine the vascular effects of combined administration of endothelin‐1 and PAF in conscious rats. Intravenous bolus injection of endothelin‐1 (0.1–2 nmol kg−1) resulted in a dose‐dependent biphasic change in mean arterial blood pressure (MABP) with initial transient hypotension followed by a prolonged pressor action. These changes were accompanied by a dose‐dependent increase in haematocrit values. Endothelin‐1 (0.1 and 1 nmol kg−1) increased dose‐dependently the vascular permeability of the trachea, upper and lower bronchi, stomach, duodenum, spleen and kidney (up to 240%) as measured by the extravasation of Evans blue dye. The permeability of pulmonary parenchyma, liver and pancreas was not affected significantly by endothelin‐1 treatment. Pretreatment of animals with the specific PAF receptor antagonist, WEB 2086 (1 mg kg−1, i.v.) or BN 52021 (10 mg kg−1, i.v.) reduced the endothelin‐1 (1 nmol kg−1)‐induced rise in haematocrit by about 50 and 30%, respectively. Both antagonists were highly effective at inhibiting protein extravasation in the stomach, duodenum and kidney. On the other hand, BN 52021, but not WEB 2086, significantly attenuated the effect of endothelin‐1 on permeability in the lower bronchi and spleen. Neither WEB 2086 nor BN 52021 modified the changes in MABP evoked by endothelin‐1. When low doses of endothelin‐1 (0.1 nmol kg−1) and PAF (0.19 nmol kg−1) were administered simultaneously, enhanced protein extravasation was detected in the upper and lower bronchi, whereas neither endothelin‐1 nor PAF by themselves affected vascular permeability in these tissues. These changes occurred in the absence of significant changes in MABP. Combined administration of higher doses of endothelin‐1 (1 nmol kg−1) and PAF (1.9 nmol kg−1) resulted in marked increases (up to 530%) in protein extravasation in the airways, pancreas, stomach and duodenum. The effect of endothelin‐1 on permeability was not affected by PAF in the spleen, whereas it was completely inhibited by PAF in the kidney. Combined injection of endothelin‐1 and PAF resulted in a slight, but significant increase in MABP. The present findings show that endothelin‐1 is capable of increasing vascular permeability in selected vascular beds including the airways, gastrointestinal tract and kidney, and suggest that PAF may mediate, in part, its action on permeability, but not its hypotensive action. The present data also suggest that endothelin‐1 and PAF can act in concert to increase vascular permeability in rat airways and gastrointestinal tract.

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“…PAF has been shown to mediate the injury in several models of gastrointestinal disease such as NEC (4) and the intestinal injury associated with hemorrhagic shock (41), mesenteric ischemia-reperfusion (33) and septic shock (42). When administered systemically to rats and mice, PAF produces a dosedependent bowel necrosis histologically resembling NEC (22).…”

Section: Discussionmentioning

confidence: 99%

Platelet-activating factor induces the processing of nuclear factor-κB p105 into p50, which mediates acute bowel injury in mice

Liu¹,

Tian²,

Baskind³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Platelet-activating factor (PAF), an endogenous proinflammatory phospholipid, when injected intravascularly to rats and mice, causes shock, acute bowel injury, and a rapid activation of NF-kappaB p50-p50 with upregulation of the chemokine CXCL2 in the intestine. In this study, we investigate the mechanism of NF-kappaB activation and the role of the NF-kappaB p50 subunit in PAF-induced shock and acute bowel injury. NF-kappaB p50-deficient mice and wild-type mice were anesthetized and tracheotomized, and their carotid artery was cannulated for blood pressure monitoring, blood sampling, and PAF administration. For determination of bowel injury, shock, and survival, PAF (2.2 microg/kg, intra-arterially, i.a.) was injected. Two hours later, animals were euthanized, and their small intestines were removed for histological examination. For biochemical studies, PAF (1.5 microg/kg i.a.) was administered and the small intestine removed after 15-60 min. We found that PAF induced an increase in p105 processing within 30 min, but there were no changes in the levels of the NF-kappaB inhibitory proteins IkappaBalpha and beta. NF-kappaB p50-deficient mice were protected against PAF-induced mortality, shock, intestinal hypoperfusion, and injury compared with wild-type animals. We also found that p50-deficient mice had decreased gene expression of CXCL2 and TNF and a decrease in CXCL2 protein production compared with wild-type mice. Our study suggests that PAF increases the processing of NF-kappaB p105 into p50, with upregulation of proinflammatory cytokines, which leads to PAF-induced systemic inflammatory response and acute bowel injury.

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Platelet-activating factor: an endogenous mediator of mesenteric ischemia-reperfusion-induced shock

Cited by 25 publications

References 0 publications

The role of cytokine-induced neutrophil chemoattractant-1 in neutrophil-mediated remote lung injury after intestinal ischaemia/reperfusion in rats

The role of cytokine-induced neutrophil chemoattractant-1 in neutrophil-mediated remote lung injury after intestinal ischaemia/reperfusion in rats

Effects of endothelin‐1 on vascular permeability in the conscious rat: interactions with platelet‐activating factor

Platelet-activating factor induces the processing of nuclear factor-κB p105 into p50, which mediates acute bowel injury in mice

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