scholarly journals Nitric oxide and renal and cardiac dysfunction in cirrhosis

2002 ◽  
Vol 102 (2) ◽  
pp. 213 ◽  
Author(s):  
Joaquín GARCÍA-ESTAÑ ◽  
M. Clara ORTIZ ◽  
Samuel S. LEE
Keyword(s):  
Nitric Oxide ◽  
Cardiac Dysfunction

scholarly journals Inorganic nitrate attenuates cardiac dysfunction: role for xanthine oxidoreductase and nitric oxide

2021 ◽  
Author(s):  
Lorna C. Gee ◽  
Gianmichele Massimo ◽  
Clement Lau ◽  
Christopher Primus ◽  
Daniel Fernandes ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Dysfunction ◽  
Xanthine Oxidoreductase ◽  
Inorganic Nitrate

A nitric oxide‐releasing derivative of enalapril, NCX 899, prevents progressive cardiac dysfunction and remodeling in hamsters with heart failure

2004 ◽  
Vol 18 (3) ◽  
pp. 587-588 ◽  
Author(s):  
Yoshitaka Iwanaga ◽  
Yusu Gu ◽  
Thomas Dieterle ◽  
Cristina Presotto ◽  
Piero Del Soldato ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Cardiac Dysfunction ◽  
Nitric Oxide Releasing

Pediatric Pulmonary Hypertension: A Pharmacotherapeutic Review

2009 ◽  
Vol 22 (2) ◽  
pp. 166-178
Author(s):  
Kimberly A. Pesaturo ◽  
Peter N. Johnson ◽  
E. Zachary Ramsey
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Cardiac Dysfunction ◽  
Dosage Forms ◽  
New Agents ◽  
The Past ◽  
Endothelin Antagonists ◽  
Pharmacological Data ◽  
Hypertension In Children ◽  
Prostacyclin Analogues

Pulmonary hypertension in children is a disorder associated with increased pulmonary vascular resistance and arterial pressure, decreased cardiac output, and right-sided cardiac dysfunction that is caused by numerous etiologies. Although treatment will vary with underlying cause, pharmacological treatment has historically included inhaled nitric oxide and prostacyclin analogues. Over the past several years new agents have been added to the treatment armamentarium, including phosphodiesterase V inhibitors (eg sildenafil) and endothelin antagonists (eg bosentan). Further, more agents are currently under investigation for pulmonary hypertension in children including immunosuppressives and other endothelin antagonist entities. Limitations to treatment include the availability of appropriate, robust pediatric pharmacological data and constraints with dosage forms.

Mechanical traumatic injury without circulatory shock causes cardiomyocyte apoptosis: role of reactive nitrogen and reactive oxygen species

2005 ◽  
Vol 288 (6) ◽  
pp. H2811-H2818 ◽  
Author(s):  
Ling Tao ◽  
Hui-Rong Liu ◽  
Feng Gao ◽  
Yan Qu ◽  
Theodore A. Christopher ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cardiac Dysfunction ◽  
Traumatic Injury ◽  
Reactive Oxygen ◽  
Cardiomyocyte Apoptosis ◽  
Reactive Nitrogen ◽  
Oxygen Species ◽  
Nitrogen Species

Apoptotic cell death plays a critical role in tissue injury and organ dysfunction under a variety of pathological conditions. The present study was designed to determine whether apoptosis may contribute to posttraumatic cardiac dysfunction, and if so, to investigate the mechanisms involved. Male adult mice were subjected to nonlethal traumatic injury, and cardiomyocyte apoptosis, cardiac function, and cardiac production of reactive oxygen/nitrogen species were determined. Modified Noble-Collip drum trauma did not result in circulatory shock, and the 24-h survival rate was 100%. No direct mechanical traumatic injury was observed in the heart immediately after trauma. However, cardiomyocyte apoptosis gradually increased and reached a maximal level 12 h after trauma. Significantly, cardiac dysfunction was observed 24 h after trauma in the isolated perfused heart. This was completely reversed when apoptosis was blocked by administration of a nonselective caspase inhibitor immediately after trauma. In the traumatized hearts, reactive nitrogen species (e.g., nitric oxide) and reactive oxygen species (e.g., superoxide) were both significantly increased, and maximal nitric oxide production preceded maximal apoptosis. Moreover, a highly cytotoxic reactive species, peroxynitrite, was markedly increased in the traumatic heart, and there was a significant positive correlation between cardiac nitrotyrosine content and caspase 3 activity. Our present study demonstrated for the first time that nonlethal traumatic injury caused delayed cell death and that apoptotic cardiomyocyte death contributes to posttrauma organ dysfunction. Antiapoptotic treatments, such as blockade of reactive nitrogen oxygen species generation, may be novel strategies in reducing posttrauma multiple organ failure.

scholarly journals Ligustrazine Attenuates Myocardial Injury Induced by Coronary Microembolization in Rats by Activating the PI3K/Akt Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Qiang Su ◽  
Xiangwei Lv ◽  
Ziliang Ye
Keyword(s):  
Nitric Oxide ◽  
Cardiac Dysfunction ◽  
Myocardial Injury ◽  
Troponin I ◽  
Interleukin 1 ◽  
Akt Pathway ◽  
Local Inflammatory Response ◽  
Coronary Microembolization ◽  
Myocardial Apoptosis ◽  
Phosphorylated Akt

Background/Aims. Coronary microembolization- (CME-) induced myocardial injury and progressive cardiac dysfunction are mainly caused due to CME-induced myocardial local inflammatory response and myocardial apoptosis. Ligustrazine plays an important protective role in multiple cardiovascular diseases, but its role and the protection mechanism in CME is unclear. This study hypothesized that ligustrazine attenuates CME-induced myocardial injury in rats. This study also explored the mechanism underlying this attenuation. Methods. Forty SD rats were randomly divided into CME group, ligustrazine group, ligustrazine+LY294002 (ligustrazine+LY) group, and sham group (ten rats in each). In each group, the cardiac function, apoptotic index, serum c-troponin I (cTnI) level, inflammation [interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α)], and oxidative stress [nitric oxide (NO), superoxide dismutase (SOD), and malondialdehyde (MDA)] were determined. Western blotting was used to detect the proteins which are present in the PI3K/Akt pathway. Results. Ligustrazine improved cardiac dysfunction induced by CME, increased serum NO and SOD activities, and decreased the serum level in IL-1β, MDA, cTnI, and TNF-α. Moreover, ligustrazine inhibited myocardial apoptosis, which is perhaps caused by the upregulated Bcl-2, the downregulated cleaved caspase-3 and Bax, and the increased protein level in endothelial nitric oxide synthase and phosphorylated Akt. These effects, however, were reduced if ligustrazine was coadministered with LY294002. Conclusions. Ligustrazine attenuates CME-induced myocardial injury. The effects associated with this attenuation may be achieved by activating the myocardium PI3K/Akt signaling pathway.

scholarly journals Cardiac Metabolism in Sepsis

Metabolites ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 846
Author(s):  
Satoshi Kawaguchi ◽  
Motoi Okada
Keyword(s):  
Nitric Oxide ◽  
Energy Metabolism ◽  
Cardiac Dysfunction ◽  
Adrenergic Receptors ◽  
Therapeutic Strategy ◽  
Cardiac Metabolism ◽  
Metabolic Abnormalities ◽  
Myocardial Energy Metabolism ◽  
Β Adrenergic Receptors ◽  
Chemical Mediators

The mechanism of sepsis-induced cardiac dysfunction is believed to be different from that of myocardial ischemia. In sepsis, chemical mediators, such as endotoxins, cytokines, and nitric oxide, cause metabolic abnormalities, mitochondrial dysfunction, and downregulation of β-adrenergic receptors. These factors inhibit the production of ATP, essential for myocardial energy metabolism, resulting in cardiac dysfunction. This review focuses on the metabolic changes in sepsis, particularly in the heart. In addition to managing inflammation, interventions focusing on metabolism may be a new therapeutic strategy for cardiac dysfunction due to sepsis.

Abstract 12692: Overexpression of Myocardial Inducible Nitric Oxide Synthase Exacerbates Cardiac Dysfunction and Beta-Adrenergic Desensitization in Streptozotocin-Induced Diabetic Mice

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yixi Liu ◽  
Che Cheng ◽  
Xiaoqiang Sun ◽  
Jing Cao ◽  
Peng Zhou ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Dysfunction ◽  
Left Ventricular ◽  
Inos Expression ◽  
Diabetic Mice ◽  
Functional Responses ◽  
Protein Levels ◽  
Wild Type Female ◽  
Inos Inhibitor ◽  
Nos Isoforms

Background: Recent evidence links impaired nitric oxide (NO) signaling pathway in the pathogenesis of diabetes-induced cardiac dysfunction. However, the different nitric oxide synthases (NOS) isoforms involved in this pathology are controversial. Recent reports have shown that in failing myocardium, increased inducible NOS (iNOS) contributes to the attenuation of β-adrenergic receptor (AR)-mediated inotropic effect. The alteration and functional significance of cardiac iNOS in diabetic cardiomyopathy (DCM) are unclear. We assessed the hypothesis that increased cardiomyocyte iNOS expression and stimulation may inhibit myocyte contraction, relaxation, [Ca 2+ ] i transient ([Ca 2+ ] iT ), and depress its response to β-AR stimulation, thereby directly contributing to the functional impairment in DCM. Methods: Left ventricular (LV) myocyte protein levels of 3 NOS and myocyte functional responses were evaluated in 2 groups of wild-type female mice (11/group): control and DCM-induced by streptozotocin (STZ) (at 10 weeks after receiving 200 mg/kg STZ, ip). In DCM, we further assessed myocyte contractile and ([Ca 2+ ] iT ) responses to β-AR stimulation by isoproterenol (ISO, 10 -8 M) with and without pretreatment of myocytes with a selective iNOS inhibitor, 1400W (10 -5 M). Results: Compared with controls, DCM myocytes had significantly increased iNOS (1.76 vs 1.03) with decreased eNOS (0.29 vs 0.34), but relatively unchanged nNOS (0.17 vs 0.18). These changes were followed by significantly reduced basal cell contraction (dL/dt max , 73.8 vs 140.7 μm/s), relaxation (dR/dt max , 61.5 vs 121.1 μm/s) and [Ca 2+ ] iT (0.17 vs 0.20). ISO-stimulated increases in dL/dt max (32% vs 59%), dR/dt max (30% vs 55%) and [Ca 2+ ] iT (17% vs 31%) were also significantly reduced. Moreover, in DCM myocytes, pretreatment with 1400W markedly improved myocyte basal contraction (128.0 μm/s) and relaxation (111.7 μm/s). The ISO-induced increases in dL/dt max (55%), dR/dt max (52%), and [Ca 2+ ] iT (29%) were also significantly augmented. Conclusions: Our findings indicate that myocardial iNOS is activated in diabetic mice and suggest that increased iNOS expression contributes to depressed myocardial contractility, impaired [Ca 2+ ] i regulation and β-adrenergic hyporesponsiveness.

Caveolin-1 peptide exerts cardioprotective effects in myocardial ischemia-reperfusion via nitric oxide mechanism

2001 ◽  
Vol 280 (6) ◽  
pp. H2489-H2495 ◽  
Author(s):  
Lindon H. Young ◽  
Yasuhiko Ikeda ◽  
Allan M. Lefer
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cardiac Dysfunction ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Polymorphonuclear Neutrophil ◽  
Caveolin 1 ◽  
Kinase C ◽  
Cardiac Contractile Dysfunction

Caveolin-1 is a protein constituent of cell membranes. The caveolin-1 scaffolding region (residues 82–101) is a known inhibitor of protein kinase C. Inhibition of protein kinase C results in maintained nitric oxide (NO) release from the endothelium, which attenuates cardiac dysfunction after ischemia-reperfusion (I/R). Therefore, we hypothesized that the caveolin-1 scaffolding region of the molecule, termed caveolin-1 peptide, might attenuate postischemia polymorphonuclear neutrophil (PMN)-induced cardiac dysfunction. We examined the effects of caveolin-1 peptide in isolated ischemic (20 min) and reperfused (45 min) rat hearts reperfused with PMNs. Caveolin-1 peptide (165 or 330 μg) given intravenously 1 h before I/R significantly attenuated postischemic PMN-induced cardiac dysfunction, as exemplified by left ventricular developed pressure (LVDP) ( P < 0.01) and the maximal rate of develped pressure (+dP/d t max) ( P < 0.01), compared with I/R hearts obtained from rats given 0.9% NaCl. In addition, caveolin-1 peptide significantly reduced cardiac PMN infiltration from 195 ± 5 PMNs/mm2 in untreated hearts to 103 ± 5 and 60 ± 5 PMNs/mm2 in hearts from 165 and 330 μg caveolin-1 peptide-treated rats, respectively ( P < 0.01). PMN adherence to the rat coronary vasculature was also significantly reduced in rats given either 165 or 330 μg caveolin-1 peptide compared with rats given 0.9% NaCl ( P < 0.01). Moreover, caveolin-1 peptide-treated rat aortas exhibited a 2.2-fold greater basal release of NO than vehicle-treated aortas ( P < 0.01), and this was inhibited by N G-nitro-l-arginine methyl ester. These results provide evidence that caveolin-1 peptide significantly attenuated PMN-induced post-I/R cardiac contractile dysfunction in the isolated perfused rat heart, probably via enhanced release of endothelium-derived NO.

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