Effect of platelet-activating factor on leukocyte adhesion to microvascular endothelium

Dillon, P K; Fitzpatrick, Michael; Ritter, Arthur; Durán, Walter N.

doi:10.1007/bf00914318

Cited by 38 publications

(20 citation statements)

References 16 publications

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“…Intravital microscopic studies in peripheral tissues have shown that local application of PAF increases vascular See Editorial Comment, page 886 permeability, 9 causes arteriolar vasoconstriction, 10 and induces leukocyte-endothelium interactions in venules. 11 In a previous intravital microscopic study using a closed cranial window preparation in the rat, we have observed that the intra-arterial infusion of PAF into the internal carotid artery in concentrations found during shock induces leukocyte-endothelium interactions in cerebral venules independent of changes in microvascular flow or of systemic parameters such as arterial blood pressure. 12 The specificity of these effects was proven by the pretreatment of the animals with the PAF receptor antagonist WEB 2170BS, which could inhibit the PAF-induced decrease in systemic blood pressure as well as the induction of leukocyte-endothelium interactions.…”

Section: ϫ6mentioning

confidence: 99%

“…30,31 Studies with PAF antagonists have indicated a role of PAF in the activation and accumulation of leukocytes after cerebral injury. 32 In peripheral organs, PAF induces margination and adhesion of leukocytes in postcapillary venules, 11 which has been considered to be the initial step in the inflammatory reaction. 33 In contrast, a marked effect of PAF on leukocyte-endothelium interactions in the brain could not be detected in the present studies.…”

Section: Leukocyte-endothelium Interactionsmentioning

confidence: 99%

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Influence of Platelet-Activating Factor on Cerebral Microcirculation in Rats

Uhl¹,

Pickelmann²,

Röhrich³

et al. 1999

Stroke

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Background and Purpose-Platelet-activating factor (PAF) is involved in the development of secondary brain damage after ischemic and traumatic brain injury. On the basis of data from studies in peripheral organs, we hypothesized that PAF-mediated effects after cerebral injury could be secondary to alterations in cerebral microcirculation. Methods-Changes in cerebral microcirculation focusing on leukocyte-endothelium interactions were quantified with the use of a closed cranial window model in Sprague-Dawley rats (nϭ33) by means of intravital fluorescence microscopy. The brain surface was superfused with PAF in concentrations from 10 Ϫ3 (nϭ3) to 10 Ϫ12 mol/L (nϭ6) for 20 minutes (5 mL/h). Results-PAF 10Ϫ4 mol/L (nϭ4) increased the number of rolling and adherent leukocytes in venules from 9.7Ϯ0.4 to 19.7Ϯ2.3 cells/100 mm ⅐ min (PϭNS versus control) and from 2.2Ϯ0.5 to 4.3Ϯ0.7 cells/100 mm ⅐ min (PϽ0.05 versus control), respectively. Lower concentrations did not elicit leukocyte-endothelium interactions. Vessel diameters remained unchanged except for a transient increase of arteriolar diameters during superfusion with PAF 10 Ϫ4 and 10

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Section: ϫ6mentioning

confidence: 99%

Section: Leukocyte-endothelium Interactionsmentioning

confidence: 99%

Influence of Platelet-Activating Factor on Cerebral Microcirculation in Rats

Uhl¹,

Pickelmann²,

Röhrich³

et al. 1999

Stroke

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“…Platelet-activating factor (PAF) is released during inflammatory responses and can cause platelet aggregation [1], leukocyte adhesion to vascular endothelium [2, 3]and arteriolar constriction [4, 5, 6, 7]. Furthermore, many studies have shown that PAF is capable of increasing vascular permeability leading to enhanced microvascular leakage of fluid and macromolecules [3, 5, 6, 7, 8, 9, 10, 11].…”

Section: Introductionmentioning

confidence: 99%

Role of Nitric Oxide and Reactive Oxygen Species in Platelet-Activating Factor-Induced Microvascular Leakage

Klabunde

Anderson²

2002

J Vasc Res

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Platelet-activating factor (PAF), released during inflammatory responses, increases microvascular permeability to fluid and macromolecules. Previous studies in the hamster cheek pouch microcirculation have shown that PAF-induced increases in permeability can be diminished by pretreatment with a nitric oxide synthase inhibitor indicating that nitric oxide is required for PAF to cause leakage, although nitric oxide itself does not cause leakage. We evaluated the hypothesis that PAF stimulates the production of reactive oxygen species (ROS) that then react with nitric oxide to form a new species that signals the increase in vascular permeability. The hamster cheek pouch microcirculation was used to quantify the leakage of FITC-dextran following topical application of PAF. PAF-induced leakage was markedly inhibited (70%) by prior superfusion of the cheek pouch with superoxide dismutase and catalase. Superfusing the cheek pouch with ROS generated by xanthine oxidase and hypoxanthine produced leakage similar to that observed with PAF. Pretreating the cheek pouch with a nitric oxide synthase inhibitor (N^ω-nitro-L-arginine, L-NA) inhibited ROS-induced leakage by 59% and PAF-induced leakage by 64%. The effects of L-NA and superoxide dismutase plus catalase on PAF-induced leakage were not additive. Systemic administration of mercaptoethylguanidine, a peroxynitrite scavenger, inhibited PAF-induced leakage by 60%. These results suggest that PAF-induced leakage may be mediated by an interaction between ROS and NO, perhaps through the formation of peroxynitrite or one of its products.

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“…In addition, like we see in MgD, PAF produces vasoconstriction of blood vessels and a variety of VSM types [for recent review, see 69], as do several of the ceramides [69,74,75]. A number of investigators employing intravital microscopy techniques, similar to those used by our laboratories [76][77][78][79][80], have demonstrated that PAF increased the number of white blood cells in the microvessels concomitant with intense vasoconstriction-spasms with increasing concentrations of the putative lipid mediator (i.e., PAF), less leukocyte rolling, and increased adherence of the leukocytes to the endothelial surfaces with increases in vascular-capillary permeability [78][79][80]. Using open and closed chambers implanted in rodent cerebral cortex and skeletal muscles, as mentioned above, we have observed similar phenomena [69].…”

Section: Is the Mysterious Intermediary Molecule Possibly Related To mentioning

confidence: 99%

Potential Roles of Magnesium Deficiency in Inflammation and Atherogenesis: Importance and Cross-talk of Platelet-Activating Factor and Ceramide

Bm¹

2016

J Clin Exp Cardiolog

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Epidemiologic studies in North America and Europe have shown that people consuming Western-type diets are low in magnesium (Mg) content (i.e., < 30 -65% of the RDA for Mg); most such diets in the USA show that 60 -80% of Americans are consuming only 185 -235 mg/day of Mg. Low Mg content in areas of soft-water, and Mg-poor soil, is associated with high incidences of ischemic heart disease (IHD), coronary artery disease, hypertension, and sudden cardiac death (SCD). It is clear that the leading underlying cause of death worldwide is atherosclerosis. Importantly, both animal and human studies have shown an inverse relationship between dietary intake of Mg and atherosclerosis. The myocardial level of Mg has consistently been observed to be lower in subjects dying from IHD and SCD in soft-water areas than those in hard-water areas. Over the past 20 years, our laboratories, using several types of primary cultured vascular smooth muscle (VSM) cells, and myocardial cells, demonstrated that declining levels of extracellular Mg ([Mg 2+ ] 0 ) activated several enzymatic pathways to produce increases in cellular sphingolipids, particularly ceramides which are known to exert numerous types of cardiovascular manifestations including inflammatory effects ; the latter play important roles in atherogenesis and cardiovascular diseases. Approximately 20 years ago, we reported that low [Mg 2+ ] 0 caused formation of platelet-activating factor (PAF) as well as other types of PAF-like molecules and suggested that these molecules might be causative agents in low Mg 2+ -induced IHD and SCD. Herein, we review results and data from our labs which strongly support roles for ceramides, PAF and PAF-like lipids in low [Mg 2+ ] 0 -induced IHD and SCD.

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Effect of platelet-activating factor on leukocyte adhesion to microvascular endothelium

Cited by 38 publications

References 16 publications

Influence of Platelet-Activating Factor on Cerebral Microcirculation in Rats

Influence of Platelet-Activating Factor on Cerebral Microcirculation in Rats

Role of Nitric Oxide and Reactive Oxygen Species in Platelet-Activating Factor-Induced Microvascular Leakage

Potential Roles of Magnesium Deficiency in Inflammation and Atherogenesis: Importance and Cross-talk of Platelet-Activating Factor and Ceramide

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