Mito-targeted antioxidant prevents cardiovascular remodelling in spontaneously hypertensive rat by modulation of energy metabolism.

Hypertension induced left ventricular hypertrophy (LVH) augments the risk of cardiovascular anomalies. Mitochondrial alterations result in oxidative stress, accompanied by decrease in fatty acid oxidation, leading to the activation of the hypertrophic program. Targeted antioxidants are expected to reduce mitochondrial reactive oxygen species more effectively than general antioxidants.

Reactivation of fatty acid oxidation by medium chain fatty acid prevents myocyte hypertrophy in H9c2 cell line.

Metabolic shift is an important contributory factor for progression of hypertension-induced left ventricular hypertrophy into cardiac failure. Under hypertrophic conditions, heart switches its substrate preference from fatty acid to glucose. Prolonged dependence on glucose for energy production has adverse cardiovascular consequences.

MR Imaging of the Hypermobile Lateral Meniscus of the Knee: A Case Report.

Objective: The hypermobile lateral meniscus of the knee is a rarely described entity. In this case report we aim to draw attention to the clinical presentation and MR imaging findings of this pathology.

Case Report: We review the clinical and imaging findings that led to the diagnosis of hypermobile lateral meniscus with transient subluxation causing intermittent locking, and which subsequently led to successful surgical treatment.

Column-Free Method for Isolation and Culture of C-Kit Positive Stem Cells from Atrial Explants.

Ever since the discovery of stem cells, their isolation from tissues and expansion in culture has been extensively studied due to its potential for therapeutic application. The magnetic-assisted cell sorting (MACS) method is the most widely used technique for the sorting of cells based on their cell surface markers. Though effective, the major drawbacks are high cost and the requirement for the frequent replacement of the columns.

Protective effect of antioxidant Tempol on cardiac stem cells in chronic pressure overload hypertrophy.

Aims: Cardiac hypertrophy, an independent risk factor for cardiac failure; is associated with oxidative stress. Decline in the proportion of healthy cardiac stem cells (CSCs), possibly mediated by oxidative stress can lead to cardiac failure. The present study was carried out to examine the hypothesis that reduction of oxidative stress restores CSC efficiency and prevents progressive cardiac remodelling.

Association of histamine with hypertension-induced cardiac remodeling and reduction of hypertrophy with the histamine-2-receptor antagonist famotidine compared with the beta-blocker metoprolol.

The association of histamine with adverse cardiac remodeling in chronic pressure overload has not received much attention. A pilot study in spontaneously hypertensive rats (SHRs) indicated a reduction of left ventricular hypertrophy (LVH) with a histamine-2-receptor (H2R) antagonist (famotidine). This finding prompted a detailed investigation of temporal variation in myocardial histamine and H2R expression and the cardiovascular response to H2R antagonism compared with that of the conventional beta-blocker metoprolol.

Modulation of cardiac stem cell characteristics by metoprolol in hypertensive heart disease.

Cardiac stem cells (CSCs) play a vital role in cardiac remodeling. Uncontrolled hypertension leads to cardiac hypertrophy, followed by cardiac failure. Pathological remodeling is associated with enhanced oxidative stress.

Accelerated decline in cardiac stem cell efficiency in Spontaneously hypertensive rat compared to normotensive Wistar rat.

Cardiac hypertrophy is recognized as an independent risk factor for cardiac failure. Efficient management of hypertensive heart disease requires identification of factors that can possibly mediate the transition from hypertrophy to failure. Resident cardiac stem cells have a prominent role in the maintenance of cardiac tissue homeostasis.

Histamine-2 receptor antagonist famotidine modulates cardiac stem cell characteristics in hypertensive heart disease.

Background: Cardiac stem cells (CSCs) play a vital role in cardiac homeostasis. A decrease in the efficiency of cardiac stem cells is speculated in various cardiac abnormalities. The maintenance of a healthy stem cell population is essential for the prevention of adverse cardiac remodeling leading to cardiac failure.

Sub-physiological oxygen levels optimal for growth and survival of human atrial cardiac stem cells.

Cardiac stem cells reside in niches where the oxygen levels are close to 3%. For cytotherapy, cells are conventionally expanded in ambient oxygen (21% O) which represents hyperoxia compared to the oxygen tension of niches. Cardiosphere-derived cells (CDCs) are then transplanted to host tissue with lower-O levels.

Association of Transforming Growth Factor-β Superfamily Genes with Non-Regression of Pulmonary Artery Hypertension Following Balloon Mitral Valvotomy: A Pilot Study.

Background And Aim Of The Study: Pulmonary arterial hypertension (PAH) is a common accompaniment of rheumatic mitral stenosis (MS), with 70% of patients showing evidence of different grades of PAH. The latter condition is found to be a prognostic factor influencing disease outcome even after interventional or surgical therapy. The cause of the non-regression of PAH following successful balloon mitral valvotomy (BMV) is not clear.

Differential response of human cardiac stem cells and bone marrow mesenchymal stem cells to hypoxia-reoxygenation injury.

Cardiosphere-derived cells (CDCs) and bone marrow mesenchymal stem cells (MSCs) are popularly used in stem cell therapy for myocardial regeneration. The cell type that survives and maintains stem cell characteristics in the adverse microenvironment following ischemia-reperfusion injury is presumed to be ideal for transplantation. The study was therefore aimed at identifying the cell type with relatively greater resistance to ischemia-reperfusion injury.

Metabolic Modulation by Medium-Chain Triglycerides Reduces Oxidative Stress and Ameliorates CD36-Mediated Cardiac Remodeling in Spontaneously Hypertensive Rat in the Initial and Established Stages of Hypertrophy.

Background: Left ventricular hypertrophy (LVH) is characterized by a decrease in oxidation of long-chain fatty acids, possibly mediated by reduced expression of the cell-surface protein cluster of differentiation 36 (CD36). Spontaneously hypertensive rats (SHRs) were therefore supplemented with medium-chain triglycerides (MCT), a substrate that bypasses CD36, based on the assumption that the metabolic modulation will ameliorate ventricular remodeling.

Methods: The diet of 2-month-old and 6-month-old SHRs was supplemented with 5% MCT (Tricaprylin), for 4 months.

Mitoprotective antioxidant EUK-134 stimulates fatty acid oxidation and prevents hypertrophy in H9C2 cells.

Oxidative stress is an important contributory factor for the development of cardiovascular diseases like hypertension-induced hypertrophy. Mitochondrion is the major source of reactive oxygen species. Hence, protecting mitochondria from oxidative damage can be an effective therapeutic strategy for the prevention of hypertensive heart disease.

Ligand specific variation in cardiac response to stimulation of peroxisome proliferator-activated receptor-alpha in spontaneously hypertensive rat.

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiac failure. Reduction of LVH has beneficial effects on the heart. LVH is associated with shift in energy substrate preference from fatty acid to glucose, mediated by down regulation of peroxisome proliferator-activated receptor-alpha (PPAR-α).

Testosterone reduces vascular relaxation by altering cyclic adenosine monophosphate pathway and potassium channel activation in male Sprague Dawley rats fed a high-salt diet.

Objectives: Male gender and high-salt diet are risk factors for hypertension. The effect of chronic exposure to testosterone is an increase in vascular tone but its influence upon responses induced by other vasoactive agents is not clear. We considered the possibility of interactions between testosterone and a high-salt diet in the mechanisms that are involved in the regulation of vascular tone.

Relaxation response of abdominal aorta to androgens in orchidectomised Sprague-Dawley rats fed a high-salt diet.

Previous studies have demonstrated the acute relaxant effects of androgens on normal arterial beds, but not on any with underlying or induced pathologies. This study investigated whether the status of the gonads affects the direct actions of androgens on isolated abdominal aorta from male Sprague-Dawley rats fed a high-salt diet. A high-salt diet reduced the relaxation response to exogenous testosterone, but not to dehydroepiandrosterone (DHEA).

Cardoguard, an Ayurvedic antihypertensive formulation, prevents cardiac remodeling in spontaneously hypertensive rats by inhibition of ERK and PKCε signaling pathways.

Ayurveda is an Indian system of medicine. Despite clinical efficacy, lack of scientific validation has limited the effective use of Ayurvedic drugs. Cardoguard is an Ayurvedic antihypertensive drug formulated by Nagarjuna Herbal Concentrates Ltd.

Association of PPARα Intron 7 Polymorphism with Coronary Artery Disease: A Cross-Sectional Study.

The allelic variants of peroxisome proliferator-activated receptor alpha (PPARα) can influence the risk of coronary artery disease (CAD) by virtue of its effect on lipid metabolism. However, the role of PPARα intronic polymorphism with CAD has received little attention. The association of allelic variants G/C at intron 7 of the PPAR-alpha gene with CAD was examined in a hospital-based Indian population.

Reactivation of peroxisome proliferator-activated receptor alpha in spontaneously hypertensive rat: age-associated paradoxical effect on the heart.

Prevention of left ventricular hypertrophy remains a challenge in the prevention of hypertension-induced adverse cardiac remodeling. Cardiac hypertrophy is associated with a shift in energy metabolism from predominantly fatty acid to glucose with a corresponding reduction in the expression of fatty acid oxidation enzyme genes. Although initially adaptive, the metabolic switch seems to be detrimental in the long run.

Testosterone relaxes abdominal aorta in male Sprague-Dawley rats by opening potassium (K(+)) channel and blockade of calcium (Ca(2+)) channel.

Aim: To investigate the direct effect of testosterone and its precursor/derivative dehydroepiandrosterone (DHEA) on isolated rat abdominal aortic rings.

Materials And Methods: 3mm abdominal aortic rings that were obtained from 3 months old male Sprague-Dawley rats were suspended in organ baths containing Hepes buffered PSS bubbled with 100% oxygen. Relaxation response to testosterone and DHEA was studied in noradrenalin pre-contracted rings.

Temporal relation of cardiac hypertrophy, oxidative stress, and fatty acid metabolism in spontaneously hypertensive rat.

Left ventricular hypertrophy is an adaptive response to hypertension, and an independent clinical risk factor for cardiac failure, sudden death, and myocardial infarction. As regression of cardiac hypertrophy is associated with a lower likelihood of cardiovascular events, it is recognized as a target of antihypertensive therapy. This necessitates identification of factors associated with the initiation and progression of hypertrophy.

Multiple signaling pathways coordinately mediate reactive oxygen species dependent cardiomyocyte hypertrophy.

The heart responds to an increased demand arising due to physiological stimuli or pathological insults by hypertrophy of myocytes. Reactive oxygen species (ROS) have recently been identified as the molecular intermediates in the translation of mechanical stimuli to cellular response. Different signal transduction pathways have been implicated with cardiac hypertrophy, prominent among them being, mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and calcineurin.

Isolation of ckit-positive cardiosphere-forming cells from human atrial biopsy.

There is increasing interest in developing cell-based therapies to regenerate functional muscle and blood vessels in infarcted dysfunctional myocardium, using stem cells resident in the adult heart. The objective of our study was to identify an easy and cost-effective method for the isolation and expansion of human adult cardiac-resident stem cells. The cells were isolated from right atrial biopsy samples obtained from patients with ischemic heart disease, who were undergoing coronary artery bypass grafting.