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Reactive oxygen species as mediators of oxygen signaling during fetal-to-neonatal circulatory transition.
Villamor, E, Moreno, L, Mohammed, R, Pérez-Vizcaíno, F, Cogolludo, A
Free radical biology & medicine. 2019;:82-96
Abstract
Reactive oxygen species (ROS) are frequently seen as pathological agents of oxidative stress. However, ROS are not always deleterious and can also act as cell signaling molecules. Vascular oxygen sensing and signaling during fetal-to-neonatal circulatory transition is a remarkable example of the physiological regulatory actions of ROS. The fetal relative hypoxic environment induces hypoxic pulmonary vasoconstriction (HPV) and ductus arteriosus (DA) relaxation favoring the presence of high pulmonary vascular resistance and right-to-left ductal shunt. At birth, the increase in oxygen tension causes relaxation of pulmonary arteries (PAs) and normoxic DA vasoconstriction (NDAV), thus diverting blood flow to the lungs. Although the response to changes in oxygen tension is diametrically opposite, the mechanisms responsible for HPV and NDAV appear to be the result of a similar interaction between triggering and modulating factors that lead to an increase in cytosolic Ca2+ concentration and Ca2+ sensitization of the contractile apparatus. Growing evidence points to an increase in ROS (mitochondria- and/or NADPH-derived superoxide and/or H2O2), leading to inhibition of voltage-gated K+ channels, membrane depolarization, and activation of voltage-gated L-type Ca2+ channels as critical events in the signaling pathway of both HPV and NDAV. Several groups of investigators have completed this pathway adding other elements such as neutral sphingomyelinase-derived ceramide, the sarcoplasmic/endoplasmic reticulum (through ryanodine and inositol 1,4,5-trisphosphate receptors), Rho kinase-mediated Ca2+ sensitization, or transient receptor potential channels. The present review focus on the role of ROS as mediators of the homeostatic oxygen sensing system during fetal and neonatal life not only in the PAs and DA but also in systemic arteries.
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2.
The role of genetics in pulmonary arterial hypertension.
Ma, L, Chung, WK
The Journal of pathology. 2017;(2):273-280
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Abstract
Group 1 pulmonary hypertension or pulmonary arterial hypertension (PAH) is a rare disease characterized by proliferation and occlusion of small pulmonary arterioles, leading to progressive elevation of pulmonary artery pressure and pulmonary vascular resistance, and right ventricular failure. Historically, it has been associated with a high mortality rate, although, over the last decade, treatment has improved survival. PAH includes idiopathic PAH (IPAH), heritable PAH (HPAH), and PAH associated with certain medical conditions. The aetiology of PAH is heterogeneous, and genetics play an important role in some cases. Mutations in BMPR2, encoding bone morphogenetic protein receptor 2, a member of the transforming growth factor-β superfamily of receptors, have been identified in 70% of cases of HPAH, and in 10-40% of cases of IPAH. Other genetic causes of PAH include mutations in the genes encoding activin receptor-like type 1, endoglin, SMAD9, caveolin 1, and potassium two-pore-domain channel subfamily K member 3. Mutations in the gene encoding T-box 4 have been identified in 10-30% of paediatric PAH patients, but rarely in adults with PAH. PAH in children is much more heterogeneous than in adults, and can be associated with several genetic syndromes, congenital heart disease, pulmonary disease, and vascular disease. In addition to rare mutations as a monogenic cause of HPAH, common variants in the gene encoding cerebellin 2 increase the risk of PAH by approximately two-fold. A PAH panel of genes is available for clinical testing, and should be considered for use in clinical management, especially for patients with a family history of PAH. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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3.
Eating and arterial endothelial function: a meta-analysis of the acute effects of meal consumption on flow-mediated dilation.
Thom, NJ, Early, AR, Hunt, BE, Harris, RA, Herring, MP
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2016;(11):1080-1090
Abstract
Given that endothelial dysfunction precedes atherosclerotic cardiovascular disease, exploring the parameters that modify postprandial flow-mediated dilation (FMD) is important for public health. The objectives of the study are to estimate the population effect of meal ingestion on FMD and to determine how the effect varied based on patient characteristics and modifiable methodological features. Articles published before June 2015 were located using MEDLINE, PubMed and Web of Science. One hundred fifty-four effects were derived from 78 articles involving 2,548 subjects were selected. Included articles required measurement of FMD in adults before and after meal ingestion. Effects were analysed using an unstandardized mean gain random effects model, and significant moderators were analysed using meta-regression. Meal consumption significantly reduced FMD by a heterogeneous mean effect size delta (Δ) of -2.03 (95% CI: [-2.28, -1.77]), an ~2% reduction in FMD. FMD reductions were larger among normal weight individuals, males, those with a cardio-metabolic disorder, those with elevated baseline FMD, and individuals with impaired glucose tolerance at baseline. Macronutrient meal ingestion significantly reduced FMD, an effect that was moderated by body mass index, sex and two-way interactions between disease status and both baseline FMD and baseline blood glucose levels.
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Causes of changes in carotid intima-media thickness: a literature review.
Qu, B, Qu, T
Cardiovascular ultrasound. 2015;:46
Abstract
Atherosclerosis causes significant morbidity and mortality. Carotid intima-media thickness (CIMT) predicts future cardiovascular and ischaemic stroke incidence. CIMT, a measure of atherosclerotic disease, can be reliably determined in vivo by carotid ultrasound. In this review, we determined that CIMT is associated with traditional cardiovascular risk factors such as age, sex, race, smoking, alcohol consumption, habitual endurance exercise, blood pressure, dyslipidemia, dietary patterns, risk-lowering drug therapy, glycemia, hyperuricemia, obesity-related anthropometric parameters, obesity and obesity-related diseases. We also found that CIMT is associated with novel risk factors, including heredity, certain genotypic indices, anthropometric cardiovascular parameters, rheumatoid arthritis, immunological diseases, inflammatory cytokines, lipid peroxidation, anthropometric hemocyte parameters, infectious diseases, vitamin D, matrix metalloproteinases, and other novel factors and diseases. However, the conclusions are inconsonant; the underlying causes of these associations remain to be further explored.
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5.
[Omega-3-polyunsaturated fatty acids: profs of benefit and perspectives of application].
Mazur, NA
Kardiologiia. 2012;(4):80-4
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6.
Stable angina pectoris: the medical management of symptomatic myocardial ischemia.
Parker, JD, Parker, JO
The Canadian journal of cardiology. 2012;(2 Suppl):S70-80
Abstract
Coronary artery disease (CAD) remains an important cause of morbidity and mortality and is a serious public health problem. Over the last 4 decades there have been dramatic advances in the both the prevention and treatment of CAD. The management of CAD was revolutionized by the development of effective surgical and percutaneous revascularization techniques. In this review we discuss the importance of the medical management of symptomatic, stable angina. Medical management approaches to both the treatment and prevention of symptomatic myocardial ischemia are summarized. In Canada, organic nitrates, β-adrenergic blocking agents, and calcium channel antagonists have been available for the therapy of angina for more than 25 years. All 3 classes are of proven benefit in the improvement of symptoms and exercise capacity in patients with stable angina. Although there is no clear first choice within these classes of anti-anginal agents, the presence of prior or concurrent conditions (for example, prior myocardial infarction and/or hypertension) plays an important role in the choice of anti-anginal class in individual patients. For some patients, combinations of different anti-anginal agents can be effective; however it is recommended that this approach be individualized. Although not currently available in Canada, other classes of anti-anginal agents have been developed; their mechanism of action and clinical efficacy is discussed. Patients with stable angina have an excellent prognosis. Patients in this category who obtain relief from symptomatic myocardial ischemia may do well without invasive intervention.
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7.
Sodium intake and vascular stiffness in hypertension.
Safar, ME, Temmar, M, Kakou, A, Lacolley, P, Thornton, SN
Hypertension (Dallas, Tex. : 1979). 2009;(2):203-9
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Contribution of endothelium-derived hyperpolarizing factors to the regulation of vascular tone in humans.
Bellien, J, Thuillez, C, Joannides, R
Fundamental & clinical pharmacology. 2008;(4):363-77
Abstract
Endothelium plays a crucial role in the regulation of cardiovascular homeostasis through the release of vasoactive factors. Besides nitric oxide (NO) and prostacyclin, increasing evidences show that endothelium-derived hyperpolarizing factors (EDHF) participate in the control of vasomotor tone through the activation of calcium-activated potassium channels. In humans, the role of EDHF has been demonstrated in various vascular beds including coronary, peripheral, skin and venous vessels. The mechanisms of EDHF-type relaxations identified in humans involved the release by the endothelium of hydrogen peroxide, epoxyeicosatrienoic acids (EETs), potassium ions and electronical communication through the gap junctions. The role of EETs could be particularly important because, in addition contributing to the maintenance of the basal tone and endothelium-dependent dilation of conduit arteries, these factors share many vascular protective properties of NO. The alteration of which might be involved in the physiopathology of cardiovascular diseases. The evolution of EDHF availability in human pathology is currently under investigation with some results demonstrating an increase in EDHF release to compensate the loss of NO synthesis and to maintain the endothelial vasomotor function whereas others reported a parallel decrease in NO and EDHF-mediated relaxations. Thus, the modulation of EDHF activity emerges as a new pharmacological target and some existing therapies in particular those affecting the renin-angiotensin system have already been shown to improve endothelial function through hyperpolarizing mechanisms. In this context, the development of new specific pharmacological agents especially those increasing EETs availability may help to prevent endothelial dysfunction and therefore enhance cardiovascular protection in patients.
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9.
Vascular compliance in the cardiometabolic syndrome.
Ganne, S, Winer, N
Journal of the cardiometabolic syndrome. 2008;(1):35-9
Abstract
Elevated systolic blood pressure and increased pulse pressure are important predictors of vascular stiffening (compliance), left ventricular hypertrophy, coronary heart disease, heart failure, stroke, vascular dementia, and chronic kidney disease. Advances in noninvasive methods that measure arterial stiffness have led to increased understanding of the mechanisms underlying vascular dysfunction and the development of associated risk factors. The ability to detect and monitor changes in the physical properties of arteries has the potential to allow early interventions that may prevent disease or attenuate its progression. In this paper, the authors briefly review the various methods available to measure vascular compliance and review pathologic processes that lead to insulin resistance, endothelial dysfunction, inflammation, and sympathetic activation, all of which may contribute to increased arterial stiffness in the cardiometabolic syndrome. Strategies to improve vascular compliance are also discussed.
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10.
Testing pulmonary vasoreactivity.
Oliveira, EC, Amaral, CF, Moura, MA, Campos, FT, Pauperio, HM
Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia. 2008;(10):838-44
Abstract
Pulmonary arterial hypertension is classified as idiopathic or secondary (associated with collagenoses, heart disease, portal hypertension, pulmonary thromboembolism, and pulmonary vascular diseases). Pulmonary vasoreactivity should be tested in order to define the best treatment option. Of the many drugs that have been used to test pulmonary vasoreactivity, inhaled nitric oxide is the best choice, due its specific pulmonary effect and very short half-life (5-10 s). The results of this test identify candidates for heart surgery among patients with congenital heart disease and candidates for the use of calcium antagonists among patients with other forms of pulmonary hypertension. Performing and interpreting the results of such tests are a great responsibility, since mistakes can lead to incorrect treatment decisions, resulting in the death of patients.