Pentoxifylline attenuates the increase in whole blood viscosity after transfusion

Bacher, A.; Eggensperger, Elisabeth; Koppensteiner, Renate; Mayer, N.; Klimscha, Walter

doi:10.1111/j.1399-6576.2004.00547.x

Cited by 24 publications

(6 citation statements)

References 22 publications

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“…PTX increases erythrocyte deformability, decreases platelet aggregation and decreases fibrinogen levels. 25,26 Furthermore, in an animal model, PTX was associated with increasing fibrinolytic activity in the peritoneum leading to a decrease in formation of peritoneal adhesions. 27 This may be relevant to PD as it has been shown that fibrin can induce PD-like lesions in animal models.…”

Section: Discussionmentioning

confidence: 99%

Pentoxifylline treatment and penile calcifications in men with Peyronie's disease

Smith

Shindel²,

Huang

et al. 2010

Asian J Androl

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This retrospective cohort study from a single clinical practice enrolled patients with evidence of calcified Peyronie’s disease (PD) plaques detected on penile ultrasound at the time of initial presentation. The primary objective was to describe the effect of pentoxifylline (PTX) treatment on subtunical calcifications in men with PD. A PD-specific questionnaire was administered and sonographic evaluations were performed at baseline and follow-up visits. Descriptive statistics and χ2 analysis were used to characterize the effect of PTX on calcified tunical plaques. In all, 71 men (mean age: 51.9 years) with PD and sonographic evidence of calcification were identified. Of them, 62 of these men were treated with PTX for a mean duration of 1 year, and nine with vitamin E or no treatment. Improvement or stabilization in calcium burden at follow-up was noted in 57 (91.9%) of men treated with PTX versus four (44.4%) of those not treated with PTX (P< 0.001). PTX users were much less likely to have a subjective worsening of their clinical condition (25.0% versus 78.3%, P=0.002). Treatment with PTX appeared to stabilize or reduce calcium content in PD plaques. A randomized controlled trial is warranted to further explore this effect.

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Section: Discussionmentioning

confidence: 99%

Pentoxifylline treatment and penile calcifications in men with Peyronie's disease

Smith

Shindel²,

Huang

et al. 2010

Asian J Androl

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“…The other replacement of the N-1-(CH 2 ) 4 COCH 3 group, as in the case of compound S6c, also showed an effective 50% and 77% inhibition of TNF-α and IL-8 production in LPS-stimulated Raw 264.7 and HK-2 cells. flexibility, reducing blood viscosity [1], and decreasing the potential for platelet aggregation [15].…”

Section: Introductionmentioning

confidence: 99%

Effects of 1,7-Substituted Methylxanthine Derivatives on LPS-Stimulated Expression of Cytokines and Chemokines in Raw 264.7 and HK-2 Cells

Kang

Shin²

2015

Journal of Microbiology and Biotechnology

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Chronic kidney diseases are based on uncontrolled immunological and inflammatory responses to pathophysiological renal circumstances such as glomerulonephritis, which is caused by immunological mechanisms of glomerular inflammation with increased production of renal pro-inflammatory cytokines. Pentoxifylline (PTX) exhibits anti-inflammatory properties by inhibiting cytokine and chemokine production through aggregation of erythrocytes and thrombocytes. We synthesized a series of 1,7-substituted methylxanthine derivatives by the Traube purine reaction, and the formation of purine ring was completed through nitrosation, a reduction of the nitroso to the amine by catalytic hydrogenation as derivatives of PTX. Then we studied biological activities such as renal anti-inflammatory effects of the synthesized compounds in the production of cytokines such as nitric oxide (NO), interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) and of chemokines such as monocyte chemoattractant protein-1 and IL-8 in Raw 264.7 and HK-2 cells. Renal antiinflammatory activities of this novel series of N-1 and N-7-substituted methylxanthine showed that the N-7 methyl-group-substituted analogs (S7b) showed selective 61% and 77% inhibition of the production of NO and IL-8. The other replacement of the N-1-(CH2)4COCH3 group, as in the case of compound S6c, also showed an effective 50% and 77% inhibition of TNF-α and IL-8 production in LPS-stimulated Raw 264.7 and HK-2 cells.

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“…The current authors have previously shown that the methylxanthine derivative pentoxifylline reduces alveolar fibrin deposition and vascular alveolar leakage, and prolongs survival in rats with neonatal hyperoxic lung injury [5], a suitable in vivo model for experimental BPD [6]. Pentoxifylline can exert its protective effect in inflammatory lung diseases in different ways, including: inhibition of vascular leakage; improved vascular blood flow by reducing blood viscosity and improving red blood cell flexibility by increasing membrane fluidity; and inhibition of leukocyte activation [7][8][9]. The protective effects in inflammatory lung diseases have been partially ascribed to the weak nonselective inhibition of PDEs by pentoxifylline, resulting in increased intracellular cAMP levels [10,11].…”

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confidence: 99%

Phosphodiesterase-4 inhibition attenuates pulmonary inflammation in neonatal lung injury

Visser

Walther²,

Laghmani³

et al. 2008

European Respiratory Journal

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Phosphodiesterase-4 (PDE4) inhibitors may offer novel therapeutic strategies in respiratory diseases, including asthma and chronic obstructive pulmonary disease. Therefore, selective PDE4 inhibitors may also provide a therapeutic option for very pre-term infants with bronchopulmonary dysplasia (BPD). The anti-inflammatory effect of two PDE4 inhibitors was investigated in a pre-term rat model of hyperoxia-induced lung injury.Pre-term rat pups were exposed to room air, hyperoxia, or hyperoxia and one of two PDE4 inhibitors: rolipram and piclamilast. The anti-inflammatory effects of prolonged PDE4 inhibitor therapy were investigated by studying survival, histopathology, fibrin deposition, alveolar vascular leakage and differential mRNA expression (real-time RT-PCR) of key genes involved in inflammation, alveolar enlargement, coagulation and fibrinolysis.PDE4 inhibitor therapy prolonged median survival by up to 7 days and reduced alveolar fibrin deposition, lung inflammation and vascular leakage by decreasing the influx of monocytes and macrophages and protein efflux in bronchoalveolar lavage fluid. Analysis of mRNA expression of key genes involved in experimental BPD revealed a significant PDE4 inhibitor-induced improvement of genes involved in inflammation, fibrin deposition and alveolarisation.In conclusion, phosphodiesterase-4 inhibition prolongs survival by inhibiting inflammation and reducing alveolar fibrin deposition in pre-term rat pups with neonatal hyperoxic lung injury, whereby piclamilast outperformed rolipram.

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Pentoxifylline attenuates the increase in whole blood viscosity after transfusion

Abstract: These results suggest that pentoxifylline is effective in attenuating the increase in whole blood viscosity after a transfusion of packed red-blood cells. Plasma viscosity is not influenced by pentoxifylline.

Cited by 24 publications

References 22 publications

Pentoxifylline treatment and penile calcifications in men with Peyronie's disease

Pentoxifylline treatment and penile calcifications in men with Peyronie's disease

Effects of 1,7-Substituted Methylxanthine Derivatives on LPS-Stimulated Expression of Cytokines and Chemokines in Raw 264.7 and HK-2 Cells

Phosphodiesterase-4 inhibition attenuates pulmonary inflammation in neonatal lung injury

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