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Subject: search.filters.subject.nitric oxide

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    Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart
    (INT INST ANTICANCER RESEARCH, 2020-01-01) Ustunova, Savas; Takir, Selcuk; Yilmazer, Nadim; Bulut, Huri; Altindirek, Didem; Ng, Ozden Hatirnaz; Tansel, Cihan Demirci; Dogan, B. Sonmez Uydes; Ozbek, Ugur; Armutak, Elif Ilkay; Gurevin, Ebru Gurel
    Background/Aim: This study was designed to provide further evidence for the interactions between hydrogen sulfide (H2S) and nitric oxide (NO) in ischemia/reperfiision (I/R) injury. Materials and Methods: Rat hearts were studied with the Langendorff technique using the H2S donor sodium hydrosulfide (NaHS, 40 mu M) and the cystathionine gamma-lyase (CTH or CSE) inhibitor DL-propargylglycine (PAG, 1 mM). NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 30 mg/kg, 7 days) was administered before the isolation. The hearts were homogenized for biochemical and molecular analysis. Results: NaHS reversed I/R-induced cardiac performance impairment, increased tissue nitric oxide production and decreased tissue markers for cardiac injury, while L-NAME inhibited these effects. The expression of CTH was increased with PAG, which was suppressed by L-NAME. Conclusion: H2S and NO increase each other's production suggesting their interaction and cooperation in cardioprotection against I/R injury.
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    786T/c endothelial nitric oxide synthase gene polymorphism and coronary collateral circulation
    (POLISH ACAD SCIENCES, INST IMMUNOL \& EXP THERAPY, 2016-01-01) Seckin, Satilmis; Emrah, Bozbeyoglu; Biyik, Ismail; Emre, Arugaslan; Burak, Tangurek; Azmi, Sungur; Omer, Celik; Sinan, Dagdelen
    Introduction: In this study, we investigated the association between -786T/C polymorphism of the endothelial nitric oxide (NOS3) gene in which thymidine is replaced by a cytosine at nucleotide -786 (rs 2070744) and coronary collateral circulation (CCC) in patients with stable coronary artery disease. Materials \& Methods: 286 patients having a critical stenosis (> 95\%) in at least one major epicardial coronary vessel were included in the study. CCC was defined according to the Rentrop classification (R). Patients with R0-1 CCC were included in the poor CCC group and subjects with R2-3 CCC were assigned to the good CCC group. The polymerase chain reaction method was used for genotyping. 152 patients with poor CCC and 134 patients with good CCC were examined. Results: The frequency of cytosine-cytosine (CC) and thymidine-cytosine (TC) genotypes and allele C were higher in the poor CCC group, but the difference did not reach statistical significance. In the dominant model, the frequency of CC+TC vs. thymidine-thymidine (TT) genotypes was significantly higher in the poor CCC group (67.1\% vs. 54.5\%, respectively
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    Endothelial nitric oxide synthase gene polymorphisms in patients with slow coronary flow
    (AKADEMIAI KIADO RT, 2017-01-01) Sezgin, Nurzen; Tekin, Abdullah; Atac, Fatma Belgin; Verdi, Hasibe; Sezgin, Alpay Turan
    Background and aims: The aim of this study was to explore potential associations of the intron 4 variable number of tandem repeats (VNTR) and E298A polymorphisms of the endothelial nitric oxide synthase (eNOS) gene with slow coronary flow (SCF). The association between plasma nitrate and nitrite (NOx) concentrations and eNOS gene polymorphisms was also assessed. Materials and methods: The intron 4 VNTR and E298A polymorphisms of the eNOS gene were evaluated in the isolated DNA blood samples obtained from the SCF patient group (n = 30) and healthy group consisted of age- and sex-matched controls (n = 61). Results: Plasma NOx level was significantly lower in patients with SCF than in controls. In addition, patients with SCF have significantly lower nitric oxide levels than control subjects within each genotype variants. The allele and genotyped frequencies of the eNOS intron 4 VNTR and E298A polymorphisms were similar between patients with SCF and the controls. Plasma NOx concentrations with respect to the relevant genotypes were found insignificant. Discussion and conclusion: Plasma NOx is lower in patients with SCF than in healthy subjects. Our findings may suggest the lack of association between intron 4 VNTR and E298A polymorphisms of the eNOS gene and SCF.