Platelet-Activating Factor in Hepatic Ischemia/Reperfusion Injury

Nishiyama, Raisuke; Suzuki, Shohachi; Baba, Shigeaki

doi:10.1097/00007890-199306000-00010

Cited by 30 publications

(10 citation statements)

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“…PAF, which is one of the most potent phospholipid mediators associated with inflammatory conditions such as I/R injury, is released from a wide variety of cells, including platelets, neutrophils, macrophages, and vascular endothelial cells [1]. In previous studies, it was reported that antagonizing PAF attenuated myocardial [10][11][12][13], hepatic [14][15][16][17][18], and lung [4][5][6][7][8] injury associated with I/R. In addition, Rabinovici et al [19] reported that endotoxin caused ARDS-like tung injury in PAF-primed rats.…”

Section: Discussionmentioning

confidence: 99%

FR128998 (a PAF receptor antagonist) counters the increased pulmonary vascular resistance associated with ischemia-reperfusion injury in the canine lung

Iwazaki¹,

Izumi²,

Ohwada³

et al. 2001

Int J Angiol

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Section: Discussionmentioning

confidence: 99%

FR128998 (a PAF receptor antagonist) counters the increased pulmonary vascular resistance associated with ischemia-reperfusion injury in the canine lung

Iwazaki¹,

Izumi²,

Ohwada³

et al. 2001

Int J Angiol

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“…O 2 0 production in the NS group hepatic ischemia, and it has also been shown that PAF was increased about threefold over the nonischemic level, while there may contribute to liver damage. [22][23][24][25] Despite many theo-was no significant change in the TCV group. Data represent the mean { SE from 5 to 8 rats at each time point.…”

Section: Fig 6 Omentioning

confidence: 99%

“…17,18 Althat on TNF-a. Thus, there may be other pathways though previous studies [22][23][24][25] have indicated that inhibipromoting CINC production that are independent of tion of PAF with specific PAF receptor antagonists PAF and TNF-a, because CINC levels rose despite comcould reduce reperfusion injury after hepatic ischemia, plete suppression of TNF-a production by TCV-309. it has not been fully explained how PAF acts in hepatic…”

Section: Fig 6 Omentioning

confidence: 99%

mentioning

confidence: 99%

“…17,18 PAF also consequence is multiple organ failure with a high mor-induces the production of cytokines such as TNF-a, tality rate, so there has been considerable interest in interleukin-6, and IL-8 by neutrophils, monocytes, and macrophages. [19][20][21] Previous studies performed in our laboratories 22 as well as others [23][24][25] have demonstrated Abbreviations: IR, ischemia-reperfusion; TNF-a, tumor necrosis factor a; that PAF might be generated in the liver and act as a IR injury have not been sufficiently elucidated. We hy-MPO, myeloperoxidase; MCLA, 2-methyl-6(p-methoxyphenyl)3,7-dihydroimidazo[1,2-a]pyrazin-3-one; PMA, phorbol 12-myristate 13-acetate; gro, growthpothesized that PAF might promote the production of related oncogene.…”

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Involvement of platelet-activating factor in cytokine production and neutrophil activation after hepatic ischemia-reperfusion

et al. 1996

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Although platelet-activating factor (PAF) is impli-the basis of hepatic IR injury. Recent studies in this cated as an important mediator in the pathogenesis of field have focused on the involvement of inflammatory hepatic ischemia-reperfusion (IR) injury, the precise cytokines and neutrophils. [1][2][3][4][5][6] Tumor necrosis factor a mechanism of its action has not been studied. We exam-(TNF-a) is reported to have a pivotal role in the cytoined the hypothesis that PAF may influence neutrophils kine cascade and in the activation of neutrophils, 7,8 and by promoting the production of tumor necrosis factor a it has been suggested to be involved in hepatic IR in-(TNF-a) and cytokine-induced neutrophil chemoattrac-jury. 1 In association with cytokine production, much tant (CINC), a member of the interleukin-8 (IL-8) family, attention has been devoted to the fact that IR of the and may be associated with liver and lung injury during liver, 1 gastrointestinal tract, 9 or lower torso 10 induces the early phase of reperfusion after total hepatic isch-lung injury as distant organ damage. Interleukin-8 (ILemia. Rats pretreated with a specific PAF receptor an-8) 11,12 is an inflammatory cytokine produced by the tagonist exhibited suppression of the increase in plasma stimulation of many types of cells, including mono-TNF-a and CINC levels, as well as the priming of periphcytes, macrophages, and endothelial cells, along with eral neutrophils for superoxide production after reperfusion when compared with animals pretreated with TNF-a and interleukin-1. This cytokine acts as a neuphysiological saline. These effects resulted in a reduc-trophil chemoattractant/activator and has been implition of plasma liver enzymes and of hepatic and pulmo-cated in reperfusion injury. 13 Although a rat equivalent nary neutrophil sequestration, as well as an increased of human IL-8 has not yet been identified, rat cytokinesurvival rate. There was a strong correlation between induced neutrophil chemoattractant (CINC) 14-16 is bethe time course of CINC release and hepatic or pulmo-lieved to be a counterpart of human melanoma growth nary neutrophil sequestration. We concluded that PAF stimulatory activity/growth-related oncogene (gro), activates neutrophils, either directly or by promoting which is classed as a member of the IL-8 family on the the production of TNF-a and CINC, and is involved in basis of its primary structure. However, no definitive evidence is available on the involvement of IL-8/CINC in liver and lung injury following hepatic IR. Hepatic ischemia-reperfusion (IR) injury is an ineviPlatelet-activating factor (PAF) has multiple effects table problem in liver transplantation, extensive hepa-on neutrophils including the promotion of chemotaxis tectomy, and hypovolemic shock. The most important and superoxide production, and priming. 17,18 PAF also consequence is multiple organ failure with a high mor-induces the production of cytokines such as TNF-a, tality rate, so there has been considerable interest in interleukin-6, and IL-8 b...

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The protective effects ofL-arginine after liver ischaemia/reperfusion injury in a pig model

et al. 1997

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Hepatic ischaemia/reperfusion is characterized by circulatory and metabolic derangement, liver dysfunction, and tissue damage. To evaluate the role of L‐arginine, a substrate of nitric oxide, in ischaemia/reperfusion injury, total liver ischaemia was induced for 120 min in 22 Landrace×Large White female pigs, which were randomly assigned to a treatment group (10 animals) or a control group (12 animals). An L‐arginine bolus (540 mg/kg i.v.) was administered to the treatment group 1 h before clamping the hepatic hilum, at clamping, at reperfusion, and at 1 and 2 h after reperfusion. The control animals received normal saline and an i.v. infusion. Liver function tests and analysis of serum, erythrocyte, and tissue malondialdehyde contents were performed at commencement of laparotomy, before reperfusion, and at 30 min and 7 days after reperfusion. Liver biopsies were taken at laparotomy, at 30 min, and at 7 days after reperfusion for histological and ultrastructural examination. Assessment of apoptosis included in situ end‐labelling analysis and DNA gel electrophoresis. Survival at 7 days was better in the treated animals than in the controls (9/10 vs. 7/12). Tissue malondialdehyde content, aspartate aminotransferase, and lactate dehydrogenase levels were lower in the treatment group, in which morphological changes were significantly less evident than in the controls 30 min after reperfusion. At 7 days, differences between the groups with respect to cell integrity were apparent only on ultrastructural analysis. Glycogen content, 7 days after reperfusion, was higher in the treatment group than in the controls: 70·25 per cent vs. 21·66 per cent positive hepatocytes (score 3 vs. score 1). Multiparametric analysis showed fewer apoptotic cells in the treatment group at all times. Our data show that the administration of L‐arginine reduces damage to liver tissue after ischaemia/reperfusion injury in a pig model. This may be explained not only by the known vasodilator, anti‐aggregation, and superoxide inactivation effects of increased nitric oxide release, but possibly also by some other action of L‐arginine, such as its influence on cellular metabolism. © 1997 John Wiley & Sons, Ltd.

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Platelet-Activating Factor in Hepatic Ischemia/Reperfusion Injury

Cited by 30 publications

References 0 publications

FR128998 (a PAF receptor antagonist) counters the increased pulmonary vascular resistance associated with ischemia-reperfusion injury in the canine lung

FR128998 (a PAF receptor antagonist) counters the increased pulmonary vascular resistance associated with ischemia-reperfusion injury in the canine lung

Involvement of platelet-activating factor in cytokine production and neutrophil activation after hepatic ischemia-reperfusion

The protective effects ofL-arginine after liver ischaemia/reperfusion injury in a pig model

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