Cardioprotective effects of traditional Chinese medicine Guanmaitong on acute myocardial infarction.

Guanmaitong (GMT) is a traditional Chinese herbal compound that has been used for the treatment of coronary heart disease (CHD) and other cardiovascular diseases. However, the efficacy of GMT in treating cardiovascular diseases remains unclear. The aim of the present study was to investigate the protective mechanisms and identify the targeted proteins and signaling networks associated with the physiological activity of GMT in a rat model of acute myocardial infarction (AMI).

Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model.

Diabetes mellitus (DM) increases the risk of developing atrial fibrillation (AF), but the molecular mechanisms of diabetes-induced atrial remodeling processes have not been fully characterized. The aim of this study was to examine the mechanisms underlying atrial ion channel remodeling in alloxan-induced diabetes model in rabbits. A total of 40 Japanese rabbits were randomly assigned to a control group (C), alloxan-induced diabetic group (DM), probucol-treated control group (Control-P), and probucol-treated diabetic group (DM-P).

Aliskiren protecting atrial structural remodeling from rapid atrial pacing in a canine model.

Atrial fibrillation (AF) contributing to the increasing mortality risk is the most common disease in clinical practice. Owing to the side effects and relative inefficacy of current antiarrhythmic drugs, some research focuses on renin-angiotensin-aldosterone system (RAS) for finding out the new treatment of AF. The purpose of this study is to confirm whether aliskiren as a proximal inhibitor of renin, which completely inhibits RAS, has beneficial effects on atrial structural remodeling in AF.

Cilostazol ameliorates atrial ionic remodeling in long-term rapid atrial pacing dogs.

Objective: Ionic remodeling has a close correlation with the occurrence of atrial fibrillation (AF). Atrial tachypacing remodeling is associated with characteristic ionic remodeling. The purpose of this study was to assess the efficacy of cilostazol, an oral phosphodiesterase 3 inhibitor, for preventing atrial ionic remodeling in long-term rapid atrial pacing (RAP) dogs.

Effects of the angiotensin-(1-7)/Mas/PI3K/Akt/nitric oxide axis and the possible role of atrial natriuretic peptide in an acute atrial tachycardia canine model.

Objective: To investigate the effects of the angiotensin-(1-7) signaling pathway and the possible role of atrial natriuretic peptide (ANP) on atrial electrical remodeling in canines with acute atrial tachycardia.

Methods: Forty dogs were randomly assigned to eight groups (five dogs/group): sham, paced control, paced + angiotensin-(1-7), paced + angiotensin-(1-7) + Mas inhibitor, paced + angiotensin-(1-7) + Akt inhibitor, paced + angiotensin-(1-7) + PI3K inhibitor, paced + angiotensin-(1-7) + nitric oxide (NO) inhibitor, and paced + angiotensin-(1-7) + A-71915 (ANP receptor antagonist). Rapid atrial pacing was maintained at 600 bpm for 2 h for all groups, except the sham group, and angiotensin-(1-7) (6 μg kg(-1) h(-1)), Mas inhibitor (5.

Protective effects of aliskiren on atrial ionic remodeling in a canine model of rapid atrial pacing.

Purpose: Aliskiren inhibits the activation of the renin-angiotensin system. Here, we investigated the effects of aliskiren on chronic atrial iron remodeling in the experimental canine model of rapid atrial pacing.

Methods: Twenty-eight dogs were assigned to sham (S), control paced (C), paced + aliskiren (10 mg Kg(-1) d(-1), A1), and paced + aliskiren (20 mg Kg(-1) d(-1), A2) groups.

Hyperglycemia aggravates atrial interstitial fibrosis, ionic remodeling and vulnerability to atrial fibrillation in diabetic rabbits.

Objective: The purpose of this study was to investigate the effects of hyperglycemia on atrial interstitial fibrosis, ionic remodeling and vulnerability to atrial fibrillation (AF) in alloxan-induced diabetic rabbits.

Methods: Sixty Japanese rabbits were randomly assigned to alloxan-induced diabetic group (n=30) and control group (n=30). Ten rabbits in each group were respectively used to electrophysiological and histological study, patch-clamp study and Western blotting analysis.

Transplantation of healthy but not diabetic outgrowth endothelial cells could rescue ischemic myocardium in diabetic rabbits.

Objective: There are two types of endothelial progenitor cell (EPC) in circulation, early EPC and outgrowth endothelial cell (OEC). Diabetes impairs the function of EPC, but it is not clear whether transplantation of OECs can rescue ischemic myocardium in diabetes. In this study, we compared the function of diabetic and healthy OECs in vitro.

Angiotensin-(1-7) prevents atrial fibrosis and atrial fibrillation in long-term atrial tachycardia dogs.

Renin-angiotensin system (RAS) is activated in the fibrillating atria. Angiotensin-(1-7) [Ang-(1-7)] counterbalances the actions of angiotensin II (Ang II). To investigate the effects of Ang-(1-7) on the long-term atrial tachycardia-induced atrial fibrosis and atrial fibrillation (AF) vulnerability, eighteen dogs were assigned to sham group, paced group, or paced+Ang-(1-7) group, 6 dogs in each group.

Enalapril, irbesartan, and angiotensin-(1-7) prevent atrial tachycardia-induced ionic remodeling.

Background: Atrial fibrillation (AF) is associated with activation of the renin-angiotensin system (RAS) in the atria. Angiotensin-(1-7) [Ang-(1-7)] is a biologically active component of the RAS, it not only counterbalances the actions of angiotensin II (Ang II) but also is a potential inhibitor of angiotensin-converting enzyme (ACE). The purpose of this study was to investigate the effects of the ACE inhibitor enalapril, the angiotensin-receptor blocker (ARB) irbesartan, and Ang-(1-7) on the chronic atrial ionic remodeling.

Atrial electrical remodeling in a canine model of sinus node dysfunction.

Aims: To study atrial tachycardia-induced electrical remodeling in a canine model of sinus node dysfunction (SND).

Materials And Methods: A canine model of SND was established by contacting a cotton patch with 20% formaldehyde on the sinus node. Atrial effective refractory period (ERP), ERP dispersion, and inducibility of atrial fibrillation (AF) were recorded at multiple sites in the atrium, before and after SND induction as well as after rapid atrial pacing.

Anti-oxidant effects of atorvastatin in dexamethasone-induced hypertension in the rat.

1. Dexamethasone (Dex)-induced hypertension is characterized by endothelial dysfunction associated with nitric oxide (NO) deficiency and increased superoxide (O2-) production. Atorvastatin (Ato) possesses pleiotropic properties that have been reported to improve endothelial function through increased availability of NO and reduced O2- production in various forms of hypertension.

Atorvastatin prevented and reversed dexamethasone-induced hypertension in the rat.

To assess the antioxidant effects of atorvastatin (atorva) on dexamethasone (dex)-induced hypertension, 60 male Sprague-Dawley rats were treated with atorva 30 mg/kg/day or tap water for 15 days. Dex increased systolic blood pressure (SBP) from 109 +/- 1.8 to 135 +/- 0.

Atorvastatin prevented and partially reversed adrenocorticotropic hormone-induced hypertension in the rat.

1. Adrenocorticotropic hormone (ACTH)-induced hypertension is associated with nitric oxide (NO) deficiency and increased oxidative stress. Atorvastatin (Ato), an HMG-Co-enzyme-A reductase inhibitor has been reported to enhance availability of NO.