ArticleMaedica2012
Sildenafil Reduces Inflammation and Prevents Pulmonary Arterial Remodeling of the Monocrotaline - induced Disease in the Wistar Rats.
Article in Maedica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- An overview on pharmaceutical applications of phosphodiesterase enzyme 5 (PDE5) inhibitors.Molecular diversity · 2025Review
- Tadalafil for Treatment of Fetal Growth Restriction: A Review of Experimental and Clinical Studies.Biomedicines · 2024Review
- Function of sildenafil on diseases other than urogenital system: An umbrella review.Frontiers in pharmacology · 2023Article
- Erectile Dysfunction in Men with Chronic Obstructive Pulmonary Disease.Journal of clinical medicine · 2021Review
- Metformin prevents the development of monocrotaline-induced pulmonary hypertension by decreasing serum levels of big endothelin-1.Experimental and therapeutic medicine · 2020Article
- Design, synthesis and biological evaluation of new 2-aminothiazole scaffolds as phosphodiesterase type 5 regulators and COX-1/COX-2 inhibitors.RSC advances · 2020Article
- Sildenafil Prevents Marfan-Associated Emphysema and Early Pulmonary Artery Dilation in Mice.The American journal of pathology · 2019Article
- Recurrent inhibition of mitochondrial complex III induces chronic pulmonary vasoconstriction and glycolytic switch in the rat lung.Respiratory research · 2018Article
- Beneficial Effect ofMedicines (Basel, Switzerland) · 2018Article
- Sildenafil activates antioxidant and antiapoptotic genes and inhibits proinflammatory cytokine genes in a rat model of renal ischemia/reperfusion injury.International urology and nephrology · 2015Article
- The role of phosphodiesterase-5 inhibitors in prostatic inflammation: a review.Journal of inflammation (London, England) · 2015Review
- The role of phosphodiesterase inhibitors in the management of pulmonary vascular diseases.Global cardiology science & practice · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPulmonary arterial hypertension (PAH) is a rare and severe disease with incompletely under stood pathogenesis. PAH is associated with pulmonary arterial remodeling and inflammation. We evaluated the effects of Sildenafil on the Monocrotaline (MCT) -induced disease in Wistar rats, for potential benefit in the early phases of inflammation and vascular remodeling. MATERIAL AND
methodsMCT-injected rats, MCT-injected sildenafil-treated rats (starting day 1 with 2 x 0.2 mg/day; total of 2 mg/kgc/day) and saline-injected control rats were evaluated at day 14 and day 28 following MCT for pulmonary morphological changes - lesions, inflammation (inflammator y index), arterial morphometry (hypertrophy index), immunohistochemistry for smooth muscle cell marker. OUTCOMES: The administration of sildenafil following MCT significantly reduced the severity of inflammation in the acute stage of the disease (reduction of the inflammatory index by 6.038% (p <0.05)) and prevented pulmonary arterial remodeling (reduction of the hypertrophy index by 7.306% (p<0.001)). It also improved survival in the early phase with a mortality rate during the first 14 days of 4 in the MCT- exposed rats vs 1 in the MCT-exposed sildenafil-treated rate.
conclusionsEarly administration of sildenafil in the MCT experimental PAH improves inflammation and survival, and prevents pulmonary vascular remodeling. Our study suggests that one of the mechanisms involved, besides vasodilatation and anti-proliferative effect, could be a direct anti-inflammatory effect of sildenafil.
Indexed as
Identifiers
23400229PMC3557417W2143097300What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.