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Find video protocols related to scientific articles indexed in Pubmed.
PPAR? activation does not affect endothelin activity in non-diabetic patients with hypertension or hypercholesterolemia.
Atherosclerosis
PUBLISHED: 02-11-2014
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This study tested the hypothesis that pioglitazone reduces endothelin-1 activity in the forearm vasculature in non-diabetic patients with hypertension or hypercholesterolemia and variable degrees of insulin resistance.
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The vascular endothelin system in obesity and type 2 diabetes: Pathophysiology and therapeutic implications.
Life Sci.
PUBLISHED: 02-05-2014
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Obesity, the metabolic syndrome (MetS), and type 2 diabetes (T2DM) are associated with heightened cardiovascular risk. Given the vasoconstrictor and proatherogenic properties of endothelin (ET)-1, increased ET-1 activity has been postulated to participate in the derangement of adiposity-related vascular homeostasis. This concept is supported by human studies using receptor antagonists to show that the activity of endogenous ET-1 is indeed enhanced in overweight and obesity, the MetS, and T2DM. Also, increased ET-1 contributes to endothelial dysfunction related to obesity, the MetS, and T2DM, whereas decreasing ET-1 vasoconstrictor tone in these patients corrects the defective endothelium-dependent vasodilation. In addition, in patients with central adiposity and the MetS, enhanced intravascular ET-1 activity coexists with decreased nitric oxide (NO)-dependent vasodilator capacity, suggesting a prevalence of vasoconstrictor mediators in vessels of obese individuals. One mechanism evoked to explain the development of vascular abnormalities in obesity deals with the derangement of the physiological vascular effects of insulin in insulin-resistant states. Thus, in conditions of adiposity, defective insulin-mediated vasodilation leads to impaired ability of the hormone to enhance its delivery and that of substrates to peripheral tissues. An important role of ET-1 in this abnormality is supported by studies showing that upregulation of the ET-1 system impairs NO-mediated vasodilation in insulin-resistant patients, whereas NO bioactivity is restored following ET-1 antagonism. In conclusion, considerable evidence supports a mechanistic role of ET-1 in the pathophysiology of adiposity-related vascular dysfunction. Targeting the ET-1 system, therefore, might have the potential for effective cardiovascular prevention in obesity, the MetS, and T2DM.
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Toll-like receptor 4 mediates endothelial cell activation through NF-?B but is not associated with endothelial dysfunction in patients with rheumatoid arthritis.
PLoS ONE
PUBLISHED: 01-01-2014
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To investigate the effects of TLR4 antagonism on human endothelial cells activation and cytokine expression, and whether the Asp299Gly TLR4 polymorphism is associated with better endothelial function in patients with rheumatoid arthritis (RA).
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Soluble guanylate cyclase: a potential therapeutic target for heart failure.
Heart Fail Rev
PUBLISHED: 09-07-2013
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The number of annual hospitalizations for heart failure (HF) and the mortality rates among patients hospitalized for HF remains unacceptably high. The search continues for safe and effective agents that improve outcomes when added to standard therapy. The nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway serves an important physiologic role in both vascular and non-vascular tissues, including regulation of myocardial and renal function, and is disrupted in the setting of HF, leading to decreased protection against myocardial injury, ventricular remodeling, and the cardio-renal syndrome. The impaired NO-sGC-cGMP pathway signaling in HF is secondary to reduced NO bioavailability and an alteration in the redox state of sGC, making it unresponsive to NO. Accordingly, increasing directly the activity of sGC is an attractive pharmacologic strategy. With the development of two novel classes of drugs, sGC stimulators and sGC activators, the hypothesis that restoration of NO-sGC-cGMP signaling is beneficial in HF patients can now be tested. Characterization of these agents in pre-clinical and clinical studies has begun with investigations suggesting both hemodynamic effects and organ-protective properties independent of hemodynamic changes. The latter could prove valuable in long-term low-dose therapy in HF patients. This review will explain the role of the NO-sGC-cGMP pathway in HF pathophysiology and outcomes, data obtained with sGC stimulators and sGC activators in pre-clinical and clinical studies, and a plan for the further clinical development to study these agents as HF therapy.
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Current management and future directions for the treatment of patients hospitalized for heart failure with low blood pressure.
Heart Fail Rev
PUBLISHED: 09-07-2013
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Although patients hospitalized with heart failure have relatively low in-hospital mortality, the post-discharge rehospitalization and mortality rates remain high despite advances in treatment. Most patients admitted for heart failure have normal or high blood pressure, but 15-25 % have low systolic blood pressure with or without signs and/or symptoms of hypoperfusion. All pharmacological agents known to improve the prognosis of patients with heart failure also reduce blood pressure, and this limits their use in patients with heart failure and low blood pressure (HF-LBP). However, patients with HF-LBP have much higher in-hospital and post-discharge mortality. In these patients, a conceptually important therapeutic target is to improve cardiac output in order to alleviate signs of hypoperfusion. Accordingly, the majority of these patients will require an inotrope as cardiac dysfunction is the cause of their low cardiac output. However, the short-term use of currently available inotropes has been associated with further decreases in blood pressure and increases in heart rate, myocardial oxygen consumption and arrhythmias. Agents that improve cardiac contractility without this undesirable effects should be developed. To the best of our knowledge, the epidemiology, pathophysiology and therapy of patients with HF-LBP have not been addressed thoroughly. In June 2010, a workshop that included scientists and clinicians was held in Rome, Italy. The objectives of this meeting were to (1) develop a working definition for HF-LBP, (2) describe its clinical characteristics and pathophysiology, (3) review current therapies and their limitations, (4) discuss novel agents in development and (5) create a framework for the design and conduct of future clinical trials.
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n-3 polyunsaturated fatty acids in the prevention of atrial fibrillation recurrences after electrical cardioversion: a prospective, randomized study.
Circulation
PUBLISHED: 08-15-2011
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n-3 polyunsaturated fatty acids (n-3 PUFAs) exert antiarrhythmic effects and reduce sudden cardiac death. However, their role in the prevention of atrial fibrillation remains controversial. We aimed to determine the effect of n-3 PUFAs in addition to amiodarone and a renin-angiotensin-aldosterone system inhibitor on the maintenance of sinus rhythm after direct current cardioversion in patients with persistent atrial fibrillation.
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Changes in renal function during hospitalization and soon after discharge in patients admitted for worsening heart failure in the placebo group of the EVEREST trial.
Eur. Heart J.
PUBLISHED: 07-23-2011
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To provide an in-depth clinical characterization and analysis of outcomes of the patients hospitalized for heart failure (HF) who subsequently develop worsening renal function (WRF) during hospitalization or soon after discharge.
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Cardiovascular mortality in chronic kidney disease patients undergoing percutaneous coronary intervention is mainly related to impaired P2Y12 inhibition by clopidogrel.
J. Am. Coll. Cardiol.
PUBLISHED: 01-22-2011
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We sought to determine whether low platelet response to the P2Y(12) receptor antagonist clopidogrel as assessed by vasodilator-stimulated phosphoprotein flow cytometry test (VASP-FCT) differentially affects outcomes in patients with or without chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI).
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Effects of n-3 polyunsaturated fatty acids on left ventricular function and functional capacity in patients with dilated cardiomyopathy.
J. Am. Coll. Cardiol.
PUBLISHED: 01-06-2011
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This study was designed to test the effects of n-3 polyunsaturated fatty acids (PUFAs) on left ventricular (LV) systolic function in chronic heart failure (HF) due to nonischemic dilated cardiomyopathy (NICM).
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Acute heart failure with low cardiac output: can we develop a short-term inotropic agent that does not increase adverse events?
Curr Heart Fail Rep
PUBLISHED: 07-14-2010
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Acute heart failure represents an increasingly common cause of hospitalization, and may require the use of inotropic drugs in patients with low cardiac output and evidence of organ hypoperfusion. However, currently available therapies may have deleterious effects and increase mortality. An ideal inotropic drug should restore effective tissue perfusion by enhancing myocardial contractility without causing adverse effects. Such a drug is not available yet. New agents with different biological targets are under clinical development. In particular, istaroxime seems to dissociate the inotropic effect exerted by digitalis (inhibition of the membrane sodium/potassium adenosine triphosphatase) from the arrhythmic effect and to ameliorate diastolic dysfunction (via sarcoendoplasmic reticulum calcium adenosine triphosphatase activation). Additionally, the myosin activator omecamtiv mecarbil appears to have promising characteristics, while genetic therapy has been explored in animal studies only. Further investigations are needed to confirm and expand the effectiveness and safety of these agents in patients with acute heart failure and low cardiac output.
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Effects of GLP-1 on forearm vasodilator function and glucose disposal during hyperinsulinemia in the metabolic syndrome.
Diabetes Care
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Patients with the metabolic syndrome (MetS) have impaired insulin-induced enhancement of vasodilator responses. The incretin hormone glucagon-like peptide 1 (GLP-1), beyond its effects on blood glucose, has beneficial actions on vascular function. This study, therefore, aimed to assess whether GLP-1 affects insulin-stimulated vasodilator reactivity in patients with the MetS.
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Rho-kinase inhibition improves vasodilator responsiveness during hyperinsulinemia in the metabolic syndrome.
Am. J. Physiol. Endocrinol. Metab.
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In patients with the metabolic syndrome (MetS), the facilitatory effect of insulin on forearm vasodilator responsiveness to different stimuli is impaired. Whether the RhoA/Rho kinase (ROCK) pathway is involved in this abnormality is unknown. We tested the hypotheses that, in MetS patients, ROCK inhibition with fasudil restores insulin-stimulated vasodilator reactivity and that oxidative stress plays a role in this mechanism. Endothelium-dependent and -independent forearm blood flow responses to acetylcholine (ACh) and sodium nitroprusside (SNP), respectively, were assessed in MetS patients (n = 8) and healthy controls (n = 5) before and after the addition of fasudil (200 ?g/min) to an intra-arterial infusion of insulin (0.1 mU/kg/min). In MetS patients (n = 5), fasudil was also infused without hyperinsulinemia. The possible involvement of oxidative stress in the effect of fasudil during hyperinsulinemia was investigated in MetS patients (n = 5) by infusing vitamin C (25 mg/min). In MetS patients, compared with saline, fasudil enhanced endothelium-dependent and -independent vasodilator responses during insulin infusion (P < 0.001 and P = 0.008, respectively), but not in the absence of hyperinsulinemia (P = 0.25 and P = 0.13, respectively). By contrast, fasudil did not affect vasoreactivity to ACh and SNP during hyperinsulinemia in controls (P = 0.11 and P = 0.56, respectively). In MetS patients, fasudil added to insulin and vitamin C did not further enhance vasodilation to ACh and SNP (P = 0.15 and P = 0.43, respectively). In the forearm circulation of patients with the MetS, ROCK inhibition by fasudil improves endothelium-dependent and -independent vasodilator responsiveness during hyperinsulinemia; increased oxidative stress seems to be involved in the pathophysiology of this phenomenon.
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Targeting myocardial substrate metabolism in heart failure: potential for new therapies.
Eur. J. Heart Fail.
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The incidence and prevalence of heart failure have increased significantly over the past few decades. Available data suggest that patients with heart failure independent of the aetiology have viable but dysfunctional myocardium that is potentially salvageable. Although a great deal of research effort has focused on characterizing the molecular basis of heart failure, cardiac metabolism in this disorder remains an understudied discipline. It is known that many aspects of cardiomyocyte energetics are altered in heart failure. These include a shift from fatty acid to glucose as a preferred substrate and a decline in the levels of ATP. Despite these demonstrated changes, there are currently no approved drugs that target metabolic enzymes or proteins in heart failure. This is partly due to our limited knowledge of the mechanisms and pathways that regulate cardiac metabolism. Better characterization of these pathways may potentially lead to new therapies for heart failure. Targeting myocardial energetics in the viable and potentially salvageable tissue may be particularly effective in the treatment of heart failure. Here, we will review metabolic changes that occur in fatty acid and glucose metabolism and AMP-activated kinase in heart failure. We propose that cardiac energetics should be considered as a potential target for therapy in heart failure and more research should be done in this area.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.