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Query: UMLS:C0007222 (cardiovascular disease)
65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitochondria have long been known to play a critical role in maintaining the bioenergetic status of cells under physiological conditions. It was also recognized early in mitochondrial research that the reduction of oxygen to generate the free radical superoxide occurs at various sites in the respiratory chain and was postulated that this could lead to mitochondrial dysfunction in a variety of disease states. Over recent years, this view has broadened substantially with the discovery that reactive oxygen, nitrogen, and lipid species can also modulate physiological cell function through a process known as redox cell signaling. These redox active second messengers are formed through regulated enzymatic pathways, including those in the mitochondrion, and result in the posttranslational modification of mitochondrial proteins and DNA. In some cases, the signaling pathways lead to cytotoxicity. Under physiological conditions, the same mediators at low concentrations activate the cytoprotective signaling pathways that increase cellular antioxidants. Thus, it is critical to understand the mechanisms by which these pathways are distinguished to develop strategies that will lead to the prevention of cardiovascular disease. In this review, we describe recent evidence that supports the hypothesis that mitochondria have an important role in cell signaling, and so contribute to both the adaptation to oxidative stress and the development of vascular diseases.
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PMID:Free radicals, mitochondria, and oxidized lipids: the emerging role in signal transduction in vascular cells. 1706

There is abundant evidence for the association between erectile dysfunction (ED) and the traditional atherosclerotic risk factors, such as dyslipidemia, hypertension, glucose intolerance, and obesity, that make up the metabolic syndrome. Recent findings have demonstrated a linear relationship between the number of these risk factors and the prevalence of ED. There is also growing evidence that endothelial dysfunction characterized by decreased bioavailability of nitrogen monoxide (NO) and a proinflammatory, prothrombotic, and proliferative phenotype is the common pathogenetic pathway linking ED to peripheral vascular diseases. Since ED often occurs several years before any clinical manifestation of systemic cardiovascular disease, ED should be seen as a warning of early atherosclerotic disease and an opportunity for doctor and patient to initiate preventive measures.
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PMID:[Metabolic syndrome and erectile dysfunction. Epidemiologic associations and pathogenetic links]. 1716 Jun 68

Nitric oxide (nitrogen monoxide) (NO) plays an important role in a wide range of physiologic processes. A major mediator of endothelial function, NO regulates vasodilatory and antithrombotic actions in the vasculature and plays a role in reproductive functions, bronchodilation, bone formation, memory, insulin sensitivity, and gastrointestinal relaxation. NO is formed from NO synthase. Impaired NO bioactivity is strongly associated with endothelial dysfunction and cardiovascular disease, but is also implicated in a broad range of other disorders, including pulmonary hypertension, insulin resistance, erectile dysfunction, and preeclampsia. Numerous therapies designed to target NO are being investigated and developed, including NO donors and stimulants. The recent African-American Heart Failure Trial (A-HeFT) showed that the NO donor isosorbide dinitrate, combined with the vasodilator hydralazine, significantly reduced morbidity and mortality in black patients with moderate-to-severe heart failure. Antihypertensive drugs, including angiotensin-converting enzyme inhibitors, calcium channel blockers, and third-generation beta-blockers, are NO stimulants that have demonstrated significant improvement of endothelial function and NO bioactivity. Other cardiovascular therapies that may improve NO bioactivity include statins, l-arginine, and nonpharmacologic approaches such as exercise and dietary changes.
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PMID:Aspects of nitric oxide in health and disease: a focus on hypertension and cardiovascular disease. 1717 Jun 2

Limited evidence suggests that persons with conditions such as diabetes, hypertension, congestive heart failure, and respiratory conditions may be at increased risk of adverse cardiovascular morbidity and mortality associated with ambient air pollution. The authors collected data on over 4 million emergency department visits from 31 hospitals in Atlanta, Georgia, between January 1993 and August 2000. Visits for cardiovascular disease were examined in relation to levels of ambient pollutants by use of a case-crossover framework. Heterogeneity of risk was examined for several comorbid conditions. The results included evidence of stronger associations of dysrhythmia and congestive heart failure visits with comorbid hypertension in relation to increased air pollution levels compared with visits without comorbid hypertension; similar evidence of effect modification by diabetes and chronic obstructive pulmonary disease (COPD) was observed for dysrhythmia and peripheral and cerebrovascular disease visits, respectively. Evidence of effect modification by comorbid hypertension and diabetes was observed in relation to particulate matter less than 10 microm in aerodynamic diameter, nitrogen dioxide, and carbon monoxide, while evidence of effect modification by comorbid COPD was also observed in response to ozone levels. These findings provide further evidence of increased susceptibility to adverse cardiovascular events associated with ambient air pollution among persons with hypertension, diabetes, and COPD.
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PMID:Ambient air pollution and cardiovascular emergency department visits in potentially sensitive groups. 1719 48

There is growing evidence that altered production and/or spatio-temporal distribution of reactive oxidant species and reactive nitrosative species in blood creates oxidative and/or nitrosative stresses in the failing myocardium and endothelium. This contributes to the abnormal cardiac and vascular phenotypes that characterize cardiovascular disease. These derangements at the system level can now be interpreted at the integrated cellular and molecular levels in terms of effects on signaling elements in the heart and vasculature. The end results of nitric oxide/redox disequilibrium have implications for cardiac and vascular homeostasis and may result in the development of atherosclerosis, myocardial tissue remodelling and hypertrophy. Reactive oxygen species/reactive nitrogen species generation is also attributed to the transit from hypertrophic to apoptotic phenotypes, a possible mechanism of myocardial failure. In this review, we highlight the possible roles of altered production and/or spatio-temporal distribution of reactive oxidant species and reactive nitrosative species in blood on the pathogenesis of the failing cardiovascular system.
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PMID:Nitric oxide in blood. The nitrosative-oxidative disequilibrium hypothesis on the pathogenesis of cardiovascular disease. 1724 98

Processes for the deposition of copper films on transition metal barrier layers by means CVD using organometallic precursors are often found to lead to poor adhesion characteristics of the grown film. By means of first-principles molecular dynamics simulations, we show that the source of the problem is the strong reactivity of the surfaces toward the precursors, which decompose spontaneously upon contact with the surface leading to contamination of the interface. Our simulations consider Ti, Ta, and W as barrier layers, and Cu(hfac)-(tmvs) as precursor. In contrast, we show that surfaces of these metals properly passivated with nitrogen, in such a way that only N atoms are exposed on the surface, are much less active and do not lead to decomposition of the precursor. We propose this passivation procedure as a practical solution to the adhesion problem.
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PMID:Interaction of copper organometallic precursors with barrier layers of Ti, Ta and W and their nitrides: a first-principles molecular dynamics study. 1734 25

The development of medical devices for cardiovascular applications has suffered due to lack of understanding of why vascular wall cells act nonphysiologically when exposed to biomaterials. One possible reason might be the chemical environment associated with cardiovascular disease. An improved understanding of cellular and subcellular mechanisms may assist in future device design to account for the disease environment. Reactive oxygen and nitrogen species (ROS/RNS) are produced through normal cellular metabolism and are rendered harmless by enzymatic systems. However, during a disease process, these systems may act aberrantly, and either fail to convert ROS and RNS to harmless substances or by producing more oxidants. There is indirect evidence that the implantation of biomedical materials may also be responsible for the triggering of these aberrant pathways that may lead to the eventual failure of the device. The understanding of how the vascular environment may be changed at the subcellular level by the presence of a biomaterial is critical. In the following pages, we hope to review the current thinking within vascular biology regarding ROS and RNS, how they are measured, and how they may impact vascular cells.
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PMID:Reactive oxygen and nitrogen species: implications for cardiovascular device engineering. 1738 35

Glutathione peroxidase-1 (GPX1) represents the first identified mammalian selenoprotein, and our understanding in the metabolic regulation and function of this abundant selenoenzyme has greatly advanced during the past decade. Selenocysteine insertion sequence-associating factors, adenosine, and Abl and Arg tyrosine kinases are potent, Se-independent regulators of GPX1 gene, protein, and activity. Overwhelming evidences have been generated using the GPX1 knockout and transgenic mice for the in vivo protective role of GPX1 in coping with oxidative injury and death mediated by reactive oxygen species. However, GPX1 exerts an intriguing dual role in reactive nitrogen species (RNS)-related oxidative stress. Strikingly, knockout of GPX1 rendered mice resistant to toxicities of drugs including acetaminophen and kainic acid, known as RNS inducers. Intracellular and tissue levels of GPX1 activity affect apoptotic signaling pathway, protein kinase phosphorylation, and oxidant-mediated activation of NFkappaB. Data are accumulating to link alteration or abnormality of GPX1 expression to etiology of cancer, cardiovascular disease, neurodegeneration, autoimmune disease, and diabetes. Future research should focus on the mechanism of GPX1 in the pathogeneses and potential applications of GPX1 manipulation in the treatment of these disorders.
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PMID:Metabolic regulation and function of glutathione peroxidase-1. 1746 55

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the western world with its incidence increasing lately in developing countries. Several lines of evidence support a role for inflammation in atherogenesis. Hence, dietary micronutrients having antiinflammatory properties may have a potential beneficial effect with regard to CVD. Vitamin E is a potent antioxidant with antiinflammatory properties. It comprises eight different isoforms: four tocopherols (T) (alpha, beta, gamma, and delta) and four tocotrienols (T3) (alpha, beta, gamma, and delta). A wealth of data is available for the preventive efficacy of alpha-T. alpha-T supplementation in human subjects and animal models has been shown to be antioxidant and antiinflammatory in terms of decreasing C-reactive protein (CRP) and release of proinflammatory cytokines, the chemokine IL-8 and PAI-1 levels especially at high doses. gamma-T is effective in decreasing reactive nitrogen species and also appears to have antiinflammatory properties; however, there are scanty data examining pure gamma-T preparations. Furthermore, tocotrienols (alpha and gamma) also have implications for prevention of CVD; however, there are conflicting and insufficient data in the literature with regards to their potency. In this chapter, we have gathered recent emerging data on alpha-T specifically and also have given a composite view of gamma-T and tocotrienols especially with regards to their effect on inflammation as it relates to CVD.
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PMID:Vitamin E: inflammation and atherosclerosis. 1762 88

The nitrogen doped multiwalled carbon nanotubes (MWNTs) were synthesized by microwave plasma chemical vapor deposition (MPCVD) technique. In this paper, we report the results of FTIR, Raman, and TGA studies to confirm the presence of N-doping inside carbon nanotubes. Fourier transform infrared (FTIR) studies were carried out in the range 400-4000 cm(-1) to study the attachment of nitrogen impurities on carbon nanotubes. FTIR spectra of the virgin sample of MWNTs show dominant peaks which are corresponding to Si-O, C-N, N-CH3, CNT, C-O, and C-Hx, respectively. The Si-O peak has its origin in silicon substrate whereas the other peaks are due to the precursor gases present in the gas mixture. The peaks are sharp and highly intense showing the chemisorption nature of the dipole bond. The intensity of the peaks due to N-CH3, C-N, and C-H reduces after annealing. It is interesting to note that these peaks vanish on annealing at high temperature (900 degrees C). The presence of C-N peak may imply the doping of the MWNTs with N in substitution mode. The position of this intense peak is in agreement with the reported peak in carbon nitride samples prepared by plasma CVD process, since the Raman modes are also expected to be delocalized over both carbon and nitrogen sites it was found that the intensity ratio of the D and G peaks, I(D)/I(G), varies as a function of ammonia concentration. The TGA measurements, carried out under argon flow, show that the dominant weight loss of the sample occurs in the temperature range 400-600 degrees C corresponding to the removal of the impurities and amorphous carbon.
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PMID:FTIR spectroscopy of multiwalled carbon nanotubes: a simple approach to study the nitrogen doping. 1765 47


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