Clinical Application of Superior Vena Cava Spectra in Evaluation of Pulmonary Hypertension: A Comparative Echocardiography and Catheterization Study.

This study was designed to assess whether superior vena cava (SVC) Doppler flow velocities are associated with invasive measures of pulmonary arterial pressure. Eighty patients with unrepaired congenital heart disease who underwent cardiac catheterization were included (31 men, 49 women; mean age: 37.3 ± 14.

Carotid Arterial Stiffness in Patients with Congenital Heart Disease-Related Pulmonary Hypertension Assessed with Radio Frequency Data Technique.

Background: It has been well known that pulmonary hypertension (PH) caused by congenital heart disease (CHD) leads to reduced flexibility of the small pulmonary arteries, due to hemodynamic changes in the pulmonary circulation and alterations of the vasoactive profile. However, whether CHD-related PH affects the elasticity of the systemic arteries, such as the common carotid artery (CCA), has not been fully investigated. The purpose of this study was to explore the CCA stiffness in patients with CHD-related PH using the radio frequency data technique.

Serum omentin-1 levels are inversely associated with the presence and severity of coronary artery disease in patients with metabolic syndrome.

Context: Omentin-1, an adipokine secreted from visceral adipose tissue, has been reported to be associated with coronary artery disease (CAD) and metabolic disorders.

Objective: To clarify the relationship between serum omentin-1 levels and the presence and severity of CAD in patients with metabolic syndrome (MetS).

Methods: We measured serum omentin-1 levels in 175 consecutive patients with MetS and in 46 controls.

Analysis of Doppler flow spectra of the superior vena cava in a canine model of acute thromboembolic pulmonary hypertension.

We aimed to establish a canine model of acute thromboembolic pulmonary hypertension (ATEPH) and to explore the feasibility of diagnosing pulmonary hypertension (PH) through the Doppler flow spectra of the superior vena cava (SVC). A canine model of ATEPH was developed by infusing thrombus into the right femoral vein. The pulmonary arterial pressure was simultaneously measured via a right heart catheter with the guidance of ultrasound.

[The relationship between reactive oxygen species-dependent activation of p38 MAPK and the expression of tumor necrosis factor-α in cultured cardiomyocytes].

Aim: To investigate the role of p38 mitogen-activated protein kinase(MAPK) in lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) expression in neonatal rat cardiomyocytes and to determine the relationship between reactive oxygen species (ROS) and p38 MAPK activation.

Methods: Cardiomyocytes were isolated from neonatal Sprague-Dawley rats and cultured by differential adhesion. Expression of TNF-α was determined in culture medium by ELISA.

Age-related changes in the atrial muscarinic type 2 receptor and their effects on atrial fibrillation vulnerability in rabbits.

Aging plays an important role in increased vulnerability to atrial fibrillation (AF). Mediated by activity at the muscarinic type 2 receptor (M2R), the parasympathetic nerve contributes to the onset of AF. The purpose of this study was to investigate whether aging changes the distribution of M2R in the atrial myocardium and to determine the impact of these changes on AF vulnerability.

Effects of autoantibodies against M2 muscarinic acetylcholine receptors on rabbit atria in vivo.

Background: Evidence has shown that autoantibodies against M2 muscarinic acetylcholine receptors may play a role in the development of atrial fibrillation. The goal of this study was to evaluate the effects of anti-M2 receptor autoantibodies on rabbit atria in vivo.

Methods: Rabbits were immunized monthly with a synthetic peptide corresponding to the M2 receptor.

Chymase induces profibrotic response via transforming growth factor-beta 1/Smad activation in rat cardiac fibroblasts.

Mast cell-derived chymase is implicated in myocardial fibrosis (MF), but the underlying mechanism of intracellular signaling remains unclear. Transforming growth factor-beta 1 (TGF-beta1) is identified as the most important profibrotic cytokine, and Smad proteins are essential, but not exclusive downstream components of TGF-beta 1 signaling. Moreover, novel evidence indicates that there is a cross talk between Smad and mitogen-activated protein kinase (MAPK) signaling cascade.

Toll-like receptor 4 siRNA attenuates LPS-induced secretion of inflammatory cytokines and chemokines by macrophages.

Toll-like receptor 4 (TLR4) is critical for activation of macrophages by Lipopolysaccharide (LPS). In this study, we investigated the silencing effects of TLR4-specific 21-nt small interfering RNAs (siRNA) on TLR4 expression in RAW264.7 cells.

Inhibitory effect of cyclosporin A on growth and collagen synthesis of rat cardiac fibroblasts induced by arginine vasopressin.

Aim: To investigate the effects of cyclosporin A (CsA) on growth and collagen synthesis of cardiac fibroblasts (CFs) induced by arginine vasopressin (AVP).

Methods: CFs of neonatal Sprague-Dawley rats were isolated by trypsinization and cultured; growth-arrested CFs were stimulated with 1 x 10(-7) mol x L(-1) AVP in the presence or absence of CsA (0.05, 0.

Simvastatin attenuates hypertrophic responses induced by cardiotrophin-1 via JAK-STAT pathway in cultured cardiomyocytes.

Unlabelled: Cardiotrophin-1 (CT-1) is a cytokine involved in the growth and survival of cardiac cells via activation of the Janus activated kinase/signal transducer activator of transcription (JAK/STAT). Statins, 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, have effects that extend beyond cholesterol reduction and inhibit vascular smooth muscle cell (VSMC) proliferation and cardiac hypertrophy. However, whether stains also can inhibitin vitromyocardial hypertrophy or not still remains elusive.

[Effects of simvastatin on the left ventricular hypertrophy in spontaneously hypertensive rats and its relationship with the expression of protein kinase B].

Objective: To investigate the effects of simvastatin on left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs) and its possible mechanism.

Methods: Sixteen male SHRs were randomly divided into 2 equal groups: treatment group and SHR control to be given simvastatin or glucose-normal saline by oral gavage for 10 weeks. Eight Wistar-Kyoto (WKY) rats were given normal saline as normal controls.