PGE1 and Other Prostaglandins in the Treatment of Intermittent Claudication: A Meta-analysis

Amendt, Klaus

doi:10.1177/000331970505600408

Cited by 18 publications

(9 citation statements)

References 16 publications

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“…; Syeda et al. ), might be medicinally applicable for conditions in which exogenous prostaglandins are currently used, such as glaucoma (Stjernschantz ), pulmonary artery hypertension (Gomberg‐Maitland and Olschewski ), and vascular insufficiency (Amendt ). Because we found that the PGT inhibitor T26A increased autocrine/paracrine signaling through EP 1 and EP 4 receptors only in the presence of PGT, it appears that T26A does not interact directly with these two PGE 2 receptors.…”

Section: Discussionmentioning

confidence: 99%

“…In the same way that inhibitors of neurotransmitter reuptake have been useful in the management of psychiatric diseases (Mann 2005), inhibitors of prostaglandin reuptake, by raising endogenous PG levels (Chi et al 2011;Syeda et al 2012), might be medicinally applicable for conditions in which exogenous prostaglandins are currently used, such as glaucoma (Stjernschantz 2004), pulmonary artery hypertension (Gomberg-Maitland and Olschewski 2008), and vascular insufficiency (Amendt 2005). Because we found that the PGT inhibitor T26A increased autocrine/paracrine signaling through EP 1 and EP 4 receptors only in the presence of PGT, it appears that T26A does not interact directly with these two PGE 2 receptors.…”

Section: Discussionmentioning

confidence: 99%

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Regulation of prostaglandin EP₁ and EP₄ receptor signaling by carrier‐mediated ligand reuptake

Chi

Suadicani

Schuster

2014

Pharmacology Res & Perspec

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After synthesis and release from cells, prostaglandin E2 (PGE2) undergoes reuptake by the prostaglandin transporter (PGT), followed by cytoplasmic oxidation. Although genetic inactivation of PGT in mice and humans results in distinctive phenotypes, and although experiments in localized environments show that manipulating PGT alters downstream cellular events, a direct mechanistic link between PGT activity and PGE2 (EP) receptor activation has not been made. Toward this end, we created two reconstituted systems to examine the effect of PGT expression on PGE2 signaling via two of its receptors (EP1 and EP4). In human embryonic kidney cells engineered to express the EP1 receptor, exogenous PGE2 induced a dose-dependent increase in cytoplasmic Ca2+. When PGT was expressed at the plasma membrane, the PGE2 dose–response curve was right-shifted, consistent with reduction in cell surface PGE2 availability; a potent PGT inhibitor acutely reversed this shift. When bradykinin was used to induce endogenous PGE2 release, PGT expression similarly induced a reduction in Ca2+ responses. In separate experiments using Madin–Darby Canine Kidney cells engineered to express the PGE2 receptor EP4, bradykinin again induced autocrine PGE2 signaling, as judged by an abrupt increase in intracellular cAMP. As in the EP1 experiments, expression of PGT at the plasma membrane caused a reduction in bradykinin-induced cAMP accumulation. Pharmacological concentrations of exogenous PGE2 induced EP4 receptor desensitization, an effect that was mitigated by PGT. Thus, at an autocrine/paracrine level, plasma membrane PGT regulates PGE2 signaling by decreasing ligand availability at cell surface receptors.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Regulation of prostaglandin EP₁ and EP₄ receptor signaling by carrier‐mediated ligand reuptake

Chi

Suadicani

Schuster

2014

Pharmacology Res & Perspec

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“…However the influence of prostaglandins is up till today and a debatable topic in their use for PAD treatment [17][18][19][20]. It has been established clinically that the use of prostaglandin reduces claudication, add to life quality and enhances ability to walk [19].…”

Section: Discussionmentioning

confidence: 99%

Medical Management of Peripheral Artery Disease in Patient with Diabetic Foot Ulcer: A Case Report

Babatunde¹

2017

Arc Cas Rep CMed

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Critical limb ischemia (CLI) is common in patients with peripheral artery disease (PAD) and concomitant diabetes. Minor leg or foot trauma may lead to ulceration in patients with PAD and diabetes. These patients are at risk due to microcirculation damage and associated diabetic sensory neuropathy and neuroischemia. The reduced ability to combat infection resulting from poor perfusion in patients with diabetes worsens the ulceration. A 63-year-old man presented with right foot dynia and an ulcer that had been present for 6 years. Initially the patient developed an ulcer on the plantar aspect of his right foot. The ulcer worsened and required amputation of his 1 st , 2 nd , 3 rd and 5 th toes about four years ago. Since then the ulcer was slow to heal despite debridement, courses of antibiotics and visits to diabetic foot clinic. He later presented with severe pain and was admitted for management with prostaglandin E1 (Alprostadil). There was complete healing of ischemic necrosis and ulceration in the patient treated with 60 mcg of prostaglandin E1 (Alprostaldil) in 250ml of isotonic NaCl solution q3h for 15 days.

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“…Ist eine interventionelle oder operative Therapie aus welchen Gründen auch immer nicht möglich, so kann eine Therapie mit i. v.-applizierten vasodilatorischen Prostaglandinen erwogen werden. Obwohl nur etwa 50 % auf die Therapie ansprechen, zeigte sich in einer Metaanalyse eine raschere Abheilung von Ulzera, eine Reduzierung des Ruheschmerzes und eine Reduktion der Amputationsrate [3].…”

Section: Gehtrainingunclassified

Die Rolle von Cilostazol im sequenziellen Therapiespektrum der peripheren arteriellen Verschlusskrankheit (pAVK)

Weber

Meyer

Weber

et al. 2012

Dtsch med Wochenschr

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Cilostazol (Pletal(®), UCB Pharma, Monheim, Deutschland) has been successfully established since its inauguration on the German market in 2007, which is associated with a considerable distribution, in particular, in angiologic patients. However, vascularsurgical specifics in the use of Cilostazol are still lacking. The aim of this very compact short overview is (based on a selective literature search and own clinical experiences over the years) to characterize mechanism of action, use and expectable therapeutic effect of Cilostazol in the challenging management of exclusively vascularsurgcial patients with peripheral arterial occlusion disease (PAOD). Cilostazol inhibits phosphodiesterase 3 and platelet aggregation in a reversible manner with a dose-effect association, has vasodilating potential and a positive inotropic effect but provides a selective effect on the platelets, muscle and endothelial cells of the vascular wall via an intracellular increase of cAMP; in addition, there is an antiproliferative effect, it promotes neoangiogenesis, inhibits apoptosis and generation of endothelial adhesion molecules - taken together, it can be considered antiatherogenic ("anti-arterioscleroticum"). From a clinical point of view, Cilostazol is indicated in stage IIb of PAOD (Fontaine); its recommended dosage is 2x100 (reduced in case of moderate side effects, 2x50) mg with detectable prolongation of subjective (reported by the patient) and objective walking distance (but not in smokers [!]; ABI-based measurement of the effect not suitable) and partially with an improval of the quality of life (associated with a prolonged but steadily improving therapeutic effect from the 4th to the 6th week until the 6th to the 12th month). The profile of side effects is broad but mostly short-term and dominated by headache [~ 30 %] and diarrhoea [~ 15 %]). While Cilostazol not only plays a beneficial role in the setting to be used in the primary arteriosclerotic course of PAOD (called sequential therapeutic preoperative course), it appears also to provide great effect in case of a re-manifestation of claudication (approaching stage IIb according to Fontaine's classification) after previous image-guided interventional or vascularsurgical treatment (suitable conservative mid-term intermediate therapy), i) resulting in a flexible physician's tool of the angiologic and vascularsurgical setting of an outpatient clinic, and ii) which reduces significantly the number of re-interventions or prolonges the time interval(s) in between. This might finally be relevant in the perspective for an amputation-free survival.

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PGE1 and Other Prostaglandins in the Treatment of Intermittent Claudication: A Meta-analysis

Cited by 18 publications

References 16 publications

Regulation of prostaglandin EP₁ and EP₄ receptor signaling by carrier‐mediated ligand reuptake

Regulation of prostaglandin EP₁ and EP₄ receptor signaling by carrier‐mediated ligand reuptake

Medical Management of Peripheral Artery Disease in Patient with Diabetic Foot Ulcer: A Case Report

Die Rolle von Cilostazol im sequenziellen Therapiespektrum der peripheren arteriellen Verschlusskrankheit (pAVK)

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PGE1 and Other Prostaglandins in the Treatment of Intermittent Claudication: A Meta-analysis

Cited by 18 publications

References 16 publications

Regulation of prostaglandin EP1 and EP4 receptor signaling by carrier‐mediated ligand reuptake

Regulation of prostaglandin EP1 and EP4 receptor signaling by carrier‐mediated ligand reuptake

Medical Management of Peripheral Artery Disease in Patient with Diabetic Foot Ulcer: A Case Report

Die Rolle von Cilostazol im sequenziellen Therapiespektrum der peripheren arteriellen Verschlusskrankheit (pAVK)

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Regulation of prostaglandin EP₁ and EP₄ receptor signaling by carrier‐mediated ligand reuptake

Regulation of prostaglandin EP₁ and EP₄ receptor signaling by carrier‐mediated ligand reuptake