Different Effects of E- and l-Type Prostaglandins on Human Platelet and Polymorphonuclear Cell Function

Schrör, Karsten; Hecker, G

doi:10.1007/978-3-642-71679-9_4

Cited by 12 publications

(12 citation statements)

References 14 publications

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“…PGEs but not PGI2 or iloprost have been shown to increase the cyclic AMP level in human PMN stimulated by Paf or FMLP about three to four fold at concentrations which inhibit superoxide anion generation and lysosomal enzyme release (Schror & Hecker, 1986;1987). Thus, PGEs seem to interact with the signal transduction through the plasma membrane to intracellular target sites.…”

Section: Discussionmentioning

confidence: 97%

E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B₄ by human polymorphonuclear leukocytes

Ney

Schrör

1989

British J Pharmacology

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Platelet‐activating factor (Paf) was found to stimulate leukotriene B4 release from human polymorphonuclear leukocytes (PMN). This stimulation was considerably enhanced in the presence of small amounts of exogenous arachidonic acid. Prostaglandin E2 (PGE2) and PGE1 (0.1–10 μm) inhibited this reaction dose‐dependently. No inhibition was seen with iloprost at these concentrations. The data suggest that E prostaglandins are potent inhibitors of Paf‐induced leukotriene generation by human PMNs and thus may serve as local factors controlling Paf‐mediated inflammatory reactions.

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Section: Discussionmentioning

confidence: 97%

E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B₄ by human polymorphonuclear leukocytes

Ney

Schrör

1989

British J Pharmacology

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“…Conversely, superoxide anion formation, stimulated by other agents such as zymosantreated serum, phorbol myristate acetate (PMA) or arachidonic acid, remained unaffected by PCE, treatmen t [70 -751. PGEl not only inhibits superoxide anion generation, but also FMLP-induced human neutrophil aggregation [76]. Furthermore, PGE, inhibits the lysosomal enzyme release from FMLP-or PAF-stimulated and cytochalasin B-pretreated human neutrophils [75]. Thus, PGEI seems to prevent neutrophil activation by various stimuli.…”

Section: Effects On Polymorphonucleur Neutrophilsmentioning

confidence: 98%

“…Neutrophils treated with PGEl and subsequently stimulated with zymosan, the synthetic chemotactic tripeptide N-formylmethionylleucylphenylalanine (FMLP) or platelet-activating factor (PAF) exhibit a dose-dependent inhibition of superoxide anion generation [70][71][72][73][74][75]. Reactive oxygen species have been considered as a major cause for vascular injury induced by activated neutrophils adherent to endothelial cells.…”

Section: Effects On Polymorphonucleur Neutrophilsmentioning

confidence: 99%

Prostaglandin E₁ and arterial occlusive disease: pharmacological considerations

Simmet

Peskar

1988

Eur J Clin Investigation

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“…3 In vitro studies have shown that PGE 1 inhibits radical production by neutrophils. 15,16 It has been suggested that this action might contribute to the beneficial effects of PGE 1 in the treatment of patients with peripheral arterial occlusive disease. 12,15,16 It is unknown, however, whether the inhibition of neutrophil function, shown in vitro, is also effective under clinical conditions after therapeutic administration of PGE 1 .…”

Section: Discussionmentioning

confidence: 99%

“…13 Although PGE 1 was introduced in clinical practice as early as 1973 by Carlson, the mode of action is not completely understood. 14 In experimental studies, 15,16 as well as in patients with critical limb ischemia, 17 PGE 1 has been shown to inhibit neutrophil activation. This mechanism may contribute to the therapeutic effects of PGE 1 in patients with peripheral arterial occlusive disease.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil function in peripheral arterial occlusive disease: the effects of prostaglandin E1

et al. 1998

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The role of polymorph nuclear neutrophils (PMN) in limb ischemia and reperfusion has been recognized only in recent years. The present study aimed to investigate the systemic and local (in femoral venous blood) effects of intra-arterially or intravenously applied prostaglandin E1 (PGE1) on systemic and ischemia-induced local changes in neutrophil function. Thirty patients with intermittent claudication were randomly assigned to intra-arterial or intravenous infusion of prostaglandin E1 (10 microg i.a. or 15 microg i.v. over 30 min). Prior to infusion femoral arterial and venous blood samples were obtained from the predominantly affected leg under resting conditions and immediately after a 3-min period of ischemia induced by suprasystolic thigh compression. After 24 h additional blood samples were obtained at baseline, following infusion of prostaglandin E1, and again after another 3-min period of ischemia following the prostaglandin E1 infusion. Intra-arterially administered prostaglandin E1 caused an increase in the PMN count by 3.5 +/- 2% (p<0.05) and a decrease in free oxygen radical production by 13 +/- 8% (p<0.05) measured by whole blood chemiluminescence. Additionally, a trend for lower PMN filterabilities (9 +/- 12%, NS) was observed. Intra-arterially infused prostaglandin E1 significantly reduced the ischemia-induced decrease in neutrophil filterability (arterial and venous blood difference after ischemia -- control: 22 +/- 17% (p<0.05); IA PGE1: 8 +/- 11% (NS), each compared to baseline). Intravenously administered prostaglandin E1 showed similar systemic effects as the intra-arterial application, but did not affect the ischemia-induced changes in neutrophil filterability. In conclusion, prostaglandin E1 reduces PMN activation in patients with peripheral arterial occlusive disease.

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Different Effects of E- and l-Type Prostaglandins on Human Platelet and Polymorphonuclear Cell Function

Cited by 12 publications

References 14 publications

E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B₄ by human polymorphonuclear leukocytes

E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B₄ by human polymorphonuclear leukocytes

Prostaglandin E₁ and arterial occlusive disease: pharmacological considerations

Neutrophil function in peripheral arterial occlusive disease: the effects of prostaglandin E1

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Different Effects of E- and l-Type Prostaglandins on Human Platelet and Polymorphonuclear Cell Function

Cited by 12 publications

References 14 publications

E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B4 by human polymorphonuclear leukocytes

E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B4 by human polymorphonuclear leukocytes

Prostaglandin E1 and arterial occlusive disease: pharmacological considerations

Neutrophil function in peripheral arterial occlusive disease: the effects of prostaglandin E1

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Product

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E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B₄ by human polymorphonuclear leukocytes

E‐Type prostaglandins but not iloprost inhibit platelet activating factor‐induced generation of leukotriene B₄ by human polymorphonuclear leukocytes

Prostaglandin E₁ and arterial occlusive disease: pharmacological considerations