Pentoxifylline protects splanchnic prostacyclin synthesis during mesenteric ischemia/reperfusion

Myers, Stuart I.; Horton, Jureta W.; Hernandez, R.; Walker, Paula B.; Vaughan, W. Glaze

doi:10.1016/0090-6980(94)90083-3

Cited by 25 publications

(10 citation statements)

References 27 publications

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“…Anastomotic disruption is responsible for high morbidity and mortality rates and increased risk for local tumor recurrence. [29][30][31][32][33][34][35] Several factors contribute to anastomotic failure and they are mostly related to ischemia or ischemiareperfusion events. [10][11][12][13]36,37 We hypothesized that if ischemia and reperfusion are responsible for most of the anastomotic leaks, pentoxifylline could partially reverse these adverse effects and improve anastomotic healing.…”

Section: Discussionmentioning

confidence: 99%

Effect of Pentoxifylline on the Healing of Ischemic Colorectal Anastomoses

Parra-Membríves

Ruiz-Luque

Escudero-Severín

et al. 2007

Diseases of the Colon &Amp; Rectum

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Section: Discussionmentioning

confidence: 99%

Effect of Pentoxifylline on the Healing of Ischemic Colorectal Anastomoses

Parra-Membríves

Ruiz-Luque

Escudero-Severín

et al. 2007

Diseases of the Colon &Amp; Rectum

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“…Data also showed that intravascular administration of pentoxifylline caused an increase in prostacyclin and vasodilation . This drug acts as an effective hydroxyl radical sweeper, prevents vascular endothelial damage, reduces the protein leakage from small coronary arteries, and reduces the myeloperoxidase enzyme levels as an index of tissue leukocyte aggregation …”

mentioning

confidence: 95%

“…17 Data also showed that intravascular administration of pentoxifylline caused an increase in prostacyclin and vasodilation. 8,9,14,[18][19][20] This drug acts as an effective hydroxyl radical sweeper, prevents vascular endothelial damage, reduces the protein leakage from small coronary arteries, and reduces the myeloperoxidase enzyme levels as an index of tissue leukocyte aggregation. 8,9,21,22 Several documents have also supported the potential benefit of pentoxifylline in reduction of ischemiareperfusion cell injury in animal model studies.…”

mentioning

confidence: 99%

Effect of Pentoxifylline in Ameliorating Myocardial Injury in Patients With Myocardial Infarction Undergoing Thrombolytic Therapy: A Pilot Randomized Clinical Trial

Namdar

Zohori

Aslanabadi

et al. 2017

The Journal of Clinical Pharma

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Cell death following acute myocardial infarction (MI) is the hallmark pathology of cardiovascular disease, leading to considerable mortality and morbidity. Platelet and neutrophil activation and inflammatory cytokines, prominently TNF-α, play an important role in the development of cell death. Because pentoxifylline inhibits platelet and neutrophil activation and reduces TNF-α, this study was performed to assess the potential benefit of pentoxifylline in the reduction of myocardial injury following acute MI. In this randomized clinical trial, 98 patients with acute MI were randomly divided into 2 groups. The intervention group received an oral dose of 1200 mg of pentoxifylline immediately before thrombolytic therapy (TLT). All patients received the same standard protocol for treatment of MI. Cardiac enzymes were checked over 48 hours. ST resolution was measured over 90 minutes. Then all patients were followed up for a 1-month period to assess major adverse cardiac effects (MACEs). There were no significant differences in peak levels of CPK (P = .18) and CK-MB (P = .33) between the 2 groups, whereas peak level of troponin I was significantly lower in the pentoxifylline group (16.8 ± 10.4 vs 21.3 ± 11.6; P = .048). No significant change between the groups was observed in biomarkers levels, ST segment resolution, cardiac ejection fraction, and MACEs. The results showed that pentoxifylline significantly reduced the peak value of troponin I in patients with acute MI receiving TLT. No significant change was observed in the other studied parameters. Further outcome-based studies are needed to show the clinical relevance of differences between the groups in troponin peak.

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“…However, pentoxifylline (PTX), a phosphodiesterase inhibitor that also blocks cytokine expression, has been found to be promising in small clinical trials (33). In addition to elevating intracellular cAMP, PTX increases the production of prostacyclins and vasodilatory eicosanoids (25,28) and depresses the production of TNF-␣ (35).…”

mentioning

confidence: 99%

TNF-α blockade decreases oxidative stress in the paraventricular nucleus and attenuates sympathoexcitation in heart failure rats

Guggilam¹,

Haque²,

Kerut³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

102

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Oxidative stress plays an important role in the pathophysiology of cardiovascular disease. Recent evidence suggests that cytokines induce oxidative stress and contribute to cardiac dysfunction. In this study, we investigated whether increased circulating and tissue levels of tumor necrosis factor (TNF)-alpha in congestive heart failure (CHF) modulate the expression of NAD(P)H oxidase subunits, Nox2 and its isoforms, in the paraventricular nucleus (PVN) of the hypothalamus and contribute to exaggerated sympathetic drive in CHF. Heart failure was induced in Sprague-Dawly rats by coronary artery ligation and was confirmed using echocardiography. Pentoxifylline (PTX) was used to block the production of cytokines for a period of 5 wk. CHF induced a significant increase in the production of reactive oxygen species (ROS) in the left ventricle (LV) and in the PVN. The mRNA and protein expression of TNF-alpha, Nox1, Nox2, and Nox4 was significantly increased in the LV and PVN of CHF rats. CHF also decreased ejection fraction, increased Tei index, and increased circulating catecholamines (epinephrine and norepinephrine) and renal sympathetic activity (RSNA). In contrast, treatment with PTX in CHF rats completely blocked oxidative stress and decreased the production of TNF-alpha and Nox2 isoforms both in the LV and PVN. PTX treatment also decreased catecholamines and RSNA and prevented further decrease in cardiac function. In summary, TNF-alpha blockade attenuates ROS and sympathoexcitation in CHF. This study unveils new mechanisms by which cytokines play a role in the pathogenesis of CHF, thus underscoring the importance of targeting cytokines in heart failure.

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Pentoxifylline protects splanchnic prostacyclin synthesis during mesenteric ischemia/reperfusion

Cited by 25 publications

References 27 publications

Effect of Pentoxifylline on the Healing of Ischemic Colorectal Anastomoses

Effect of Pentoxifylline on the Healing of Ischemic Colorectal Anastomoses

Effect of Pentoxifylline in Ameliorating Myocardial Injury in Patients With Myocardial Infarction Undergoing Thrombolytic Therapy: A Pilot Randomized Clinical Trial

TNF-α blockade decreases oxidative stress in the paraventricular nucleus and attenuates sympathoexcitation in heart failure rats

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