ArticleBrazilian journal of cardiovascular surgery2022
Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model.
Article in Brazilian journal of cardiovascular surgery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTo clarify the potential protective role of cilostazol on rat myocardial cells with ischemia-reperfusion injury (IRI) models.
methodsThe study was conducted with three groups of 10 Wistar rats (control group, rats without any coronary ischemia; sham group, rats with coronary ischemia but without cilostazol administration; and cilostazol group, rats with coronary ischemia and cilostazol administration). The level of myocardial injuries was measured by analyzing cardiac troponin T and creatine kinase MB levels in blood samples. In tissue samples, adenosine triphosphate (ATP), nitric oxide, superoxide dismutase (SOD), and malondialdehyde were used to determine the amount of tissue damage. Tissues were stained with hematoxylin-eosin method, and samples were examined under light microscope.
resultsThe mean level of ATP was 104.4 in the cilostazol group and 149.1 in the sham group (P=0.044). SOD level was significantly higher in the cilostazol group than in the sham group (2075.3 vs. 1783.7, P=0.043). According to histopathological examination, all samples were classified as G0 in the control group. In the sham group, one sample was categorized as G1, six samples as G2, and three samples as G3. In the cilostazol group, nine samples and one sample were categorized as G1 and G2, respectively (P=0.011).
conclusionCilostazol has beneficial effects on Wistar rats' myocardial cells in regard to decreasing inflammatory process, necrosis, and fibrosis. Our findings revealed that the use of cilostazol significantly decreased ATP and increased SOD levels in Wistar rats' myocardial cells after IRI.
Indexed as
Identifiers
What 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.