Journal of Cardiovascular Pharmacology and Therapeutics (J CARDIOVASC PHARM T)

Publisher: Hindawi Publishing Corporation, SAGE Publications

Journal description

Every informative issue of the Journal of Cardiovascular Pharmacology and Therapeutics (JCPT) offers cardiologists, clinical pharmacologists and researchers involved in disease relevant clinical and experimental investigations of newer cardiovascular drugs and other therapeutic options.

Current impact factor: 3.07

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.072
2012 Impact Factor 2.38
2011 Impact Factor 1.753
2010 Impact Factor 1.969
2009 Impact Factor 1.871
2008 Impact Factor 1.672

Impact factor over time

Impact factor

Additional details

5-year impact 1.97
Cited half-life 4.00
Immediacy index 0.54
Eigenfactor 0.00
Article influence 0.63
Website Journal of Cardiovascular Pharmacology and Therapeutics website
ISSN 1940-4034
OCLC 321528431
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

SAGE Publications

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors retain copyright
    • Pre-print on any website
    • Author's post-print on author's personal website, departmental website, institutional website or institutional repository
    • On other repositories including PubMed Central after 12 months embargo
    • Publisher copyright and source must be acknowledged
    • Publisher's version/PDF cannot be used
    • Post-print version with changes from referees comments can be used
    • "as published" final version with layout and copy-editing changes cannot be archived but can be used on secure institutional intranet
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Effective treatment of chronic lower limb ischemia is one of the most challenging issues confronting vascular surgeons. There are a number of choices available to the vascular surgeon. Open or endovascular revascularization is the treatment of choice when applicable. Current pharmacological therapies play an auxiliary role and cannot prevent disease progression. Therefore, new methods of treatment are needed. We conducted a phase 2b/3 multicenter randomized controlled clinical trial of the intramuscular transfer of a plasmid DNA encoding vascular endothelial growth factor (VEGF) 165 with cytomegalovirus promotor (CMV) in patients with atherosclerotic lower limb ischemia. A total of 100 patients were enrolled in the study, that is, 75 patients were randomized into the test group and received 2 intramuscular injections of 1.2 mg of pCMV-vegf165, 14 days apart together with standard pharmacological treatment. In all, 25 patients were randomized into the control group and received standard treatment only. The following end points were evaluated within the first 6 months of the study and during a 1.5-year additional follow-up period: pain-free walking distance (PWD), ankle-brachial index (ABI), and blood flow velocity (BFV). The pCMV-vegf165 therapy appeared to be significantly more effective than standard treatment. The PWD increased in the test group by 110.4%, 167.2%, and 190.8% at 6 months, 1 year, and 2 years after treatment, respectively. The pCMV-vegf165 intramuscular transfer caused a statistically significant increase in ABI and BFV. There were no positive results in the control group. Thus, pCMV-vegf165 intramuscular gene transfer is an effective method of treatment of moderate to severe claudication due to chronic lower limb ischemia. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 03/2015; DOI:10.1177/1074248415574336
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    ABSTRACT: To determine the effect of a high-fat meal on evacetrapib exposure at steady state in healthy participants. This was a randomized, 2-period, 2-sequence, open-label, crossover study. Patients were randomly assigned to 1 of the 2 treatment sequences in which they received evacetrapib 130 mg/d for 10 days following a 10-hour fast each day or following a high-fat breakfast each day. Plasma samples collected through 24 hours were analyzed for evacetrapib concentrations and pharmacokinetic parameter estimates including area under the concentration-time curve during a dosing interval (AUCτ), maximum observed concentration (Cmax), and time of Cmax (tmax) were calculated. Pharmacodynamic parameters, including cholesteryl ester transfer protein (CETP) activity, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol, and triglycerides, were also assessed. A total of 34 males and 6 females, mean age 41.5 years and mean body mass index 26.6 kg/m(2), were enrolled. Statistical analysis showed AUCτ was 44% higher (90% confidence interval [CI]: 29%-62%) and Cmax was 51% higher (90% CI: 28%-79%) in the fed state than in the fasted state, indicating an effect of food. Consistent with higher evacetrapib exposure, changes in HDL-C, LDL-C, and CETP activity appeared to be greater in the fed state than in the fasted state. There were no notable changes in total cholesterol or triglycerides following administration in the fed and fasted states. The 130-mg doses of evacetrapib were well tolerated with and without food. A high-fat meal increased evacetrapib mean exposure at steady state by 44% in healthy participants. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 03/2015; DOI:10.1177/1074248415575153
  • Journal of Cardiovascular Pharmacology and Therapeutics 03/2015; DOI:10.1177/1074248415574744
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    ABSTRACT: Basilar vascular smooth muscle cells (BASMCs) hyperplasia is a prominent feature of cerebrovascular remodeling and stroke during the development of hypertension. Tanshinone IIA (Tan) has been reported to exhibit a protective effect against the pathological features of hypertension. Previous studies have shown that phosphoinostitide-3 kinase (PI3K)/3'-phosphoinostitide dependent kinase (PDK1)/AKT pathway is involved in the regulation of proliferation of various cell types. Therefore, there may be a crosstalk between Tan antihypertension processes and PI3K/PDK1/AKT proliferative effect in BASMCs. To test this hypothesis, we used a 2-kidney, 2-clip hypertension model to examine the effect of Tan on PI3K/PDK1/AKT pathway by cellular, molecular, and biochemical approaches. Our results revealed that the abundance of PDK1 in plasma was paralleled with an increase in blood pressure and the cross-sectional area of basilar artery in hypertensive rats. Tan decreased blood pressure and hypertension-induced PDK1 phosphorylation but produced no effect on the phosphorylation of PI3K. Moreover, Tan attenuated endothelin 1 induced the activation of PDK1/AKT pathway in rat BASMCs. Tan could inhibit cell cycle transition by regulating the expression of cyclin D1 and p27, in turn, prevent proliferation of BASMCs. Our study provides a novel mechanism by which Tan prevents cerebrovascular cell proliferation during hypertension, and thus Tan may be a potential therapeutic agent for cerebrovascular remodeling and stroke. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 03/2015; DOI:10.1177/1074248415574743
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    ABSTRACT: Patients with the coronary slow flow phenomenon frequently experience angina episodes. The present study aimed to compare the efficacy of nicorandil versus nitroglycerin for alleviation of angina symptoms in slow flow patients. In a single-center, single-blind, parallel-design, comparator-controlled, randomized clinical trial (NCT02254252), 54 patients with slow flow and normal or near-normal coronary angiography who presented with frequent angina episodes were randomly assigned to 1-month treatment with nicorandil 10 mg, 2 times a day (n = 27) or sustained-release glyceryltrinitrate 6.4 mg 2 times a day (n =27). Frequency of angina episodes, pain intensity, and the Canadian Cardiovascular Society (CCS) grading of angina pectoris were assessed at baseline and after 1 month of treatment. In all, 25 patients in the nicorandil arm and 24 patients in the nitroglycerin arm were analyzed. After 1 month, patients treated with nicorandil had fewer angina episodes (adjusted mean number of episodes per week, nicorandil versus nitroglycerin; 1.68 ± 0.15 vs 2.29 ± 0.15, P = .007, effect size = 14.6%). Patients also reported greater reductions in pain intensity with nicorandil versus nitroglycerin (adjusted mean of self-reported pain score; 3.03 ± 0.29 vs 3.89 ± 0.30, P = .046, effect size = 8.4%). A significantly higher proportion of patients in the nicorandil arm were categorized in CCS class I (76% vs 33.3%, P = .004) or class II (16.0% vs 45.8%, P = .032). In slow flow patients, nicorandil provides better symptomatic relief of angina than nitroglycerin. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 02/2015; DOI:10.1177/1074248415571457
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    ABSTRACT: Dual antiplatelet therapy with aspirin and a P2Y12 receptor antagonist remains a mainstay in the prevention of ischemic events following coronary stent placement. Significant controversy exists regarding the optimal management of high platelet reactivity despite antiplatelet therapy; however this finding has been consistently associated with poor clinical outcomes including greater risk of stent thrombosis and myocardial infarction. Variability in antiplatelet effects of clopidogrel and prasugrel has been linked to genetic polymorphisms and potential drug-drug interactions. Both of these factors have significant influence on the cytochrome P-450 enzyme system activity of the liver responsible for their biotransformation to the active form of both drugs. Very little has been publicized regarding differences in antiplatelet effects which may be associated with conditions in which the functional capacity of the liver may be temporarily compromised. Patients who present with cardiogenic shock due to acute coronary syndromes have evidence of multiorgan dysfunction including liver dysfunction that may affect the activity of these drugs. This review aims to explore existing evidence and propose additional considerations to the selection of antiplatelet therapy in patients with cardiogenic shock who receive catheter-based revascularization and stent placement. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 02/2015; DOI:10.1177/1074248415571456
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    ABSTRACT: Dantrolene, which is primarily used to treat malignant hyperthermia, has recently been suggested for the prevention of arrhythmogenesis in various animal models. In this study, the effects of dantrolene treatment on electrophysiological properties and ventricular arrhythmias (VAs) in rats with chronic β-adrenergic receptor (β-AR) activation were investigated. Rats were randomized to treatment with saline (control group), isoproterenol (ISO; ISO group), or ISO + dantrolene (ID group) for 2 weeks. An electrophysiological study was performed to assess action potential duration restitution (APDR) and induce action potential duration (APD) alternans or VA in vitro. The protein levels of Cav1.2, sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a), and ryanodine receptor 2 (RyR2) were detected by Western blot. Compared with the control group, chronic administration of ISO significantly increased APD, the maximum slope (Smax) of APDR curve, and the spatial dispersions of Smax and APD (all P < .01), and all effects were attenuated by dantrolene treatment (all P < .05). Additionally, chronic ISO administration significantly reduced the protein levels of SERCA2 and RyR2, but increased the Cav1.2 protein expression (all P < .05). However, compared with the ISO group, dantrolene treatment preserved SERCA2a and RyR2 protein levels and decreased Cav1.2 protein levels in the ID group (all P < .05). The intracellular Ca(2+) ([Ca(2+)]i) levels measured by incubating isolated cardiomyocytes with Fluo-3/alveolar macrophages were significantly increased in the ISO group compared with the control group (P < .01). Dantrolene treatment markedly reduced the rise of [Ca(2+)]i levels caused by chronic administration of ISO (P < .05). Dantrolene treatment also prevented the reductions in the APD alternans and VA thresholds induced by chronic ISO stimulation (all P < .05). These data suggest that dantrolene stabilizes ventricular electrophysiological characteristics and increases the expression of key sarcoplasmic reticulum calcium cycling proteins to reduce vulnerability to VA in rats with chronic β-AR activation. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 01/2015; DOI:10.1177/1074248414568194
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    ABSTRACT: Combination therapy is commonly used for pulmonary arterial hypertension (PAH) treatment. We aimed to identify factors that may predict the need for future combination therapy. We conducted a retrospective chart review of consecutive patients with PAH in an aim to describe baseline clinical, echocardiogram, and hemodynamic characteristics of patients who eventually required combination therapy during the course of their disease and compared them to the ones who were maintained on monotherapy. The monotherapy group was followed for an average of 31.8 ± 18.8 months and the combination therapy group was followed for an average of 28.7 ± 13.6 months. Among the 71 patients analyzed, a significantly higher number of patients who eventually required combination therapy belonged to World Health Organization functional class 3 (45% vs 37%) and 4 (23% vs 0) at baseline, compared with those on monotherapy (P < .05). Combination group also had a higher Registry to Evaluate Early And Long-term PAH Disease Management (REVEAL) PAH risk score at presentation. End of 6-minute walk test (6MWT), oxygen saturation (Spo 2) was also lower in the combination therapy group, 86% ± 8% versus 91% ± 7% (P < .05). Patients who eventually required combination therapy were more frequently noticed to have right ventricular enlargement, right atrial enlargement, and had a higher resting estimated right ventricular systolic pressure (RVSP). Right heart catheterization-derived hemodynamics data at baseline showed that the combination therapy group had a higher mean pulmonary artery (PA) pressure, lower pulmonary capillary wedge pressure, lower cardiac output, and higher pulmonary vascular resistance (PVR). On univariate analysis, only PVR ≥300 dyne·s/cm(5), mean PA pressure of ≥40 mm Hg, estimated RVSP ≥ 60 mm Hg, PAH risk score ≥ 10, and end of 6MWT saturation of ≤ 90% were of significance. Patients with PAH who require combination therapy in the course of their disease have worse hemodynamics, PAH risk score, functional class, and end of 6MWT oxygen saturation at the time of presentation compared to patients maintained on monotherapy. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 01/2015; DOI:10.1177/1074248414568195
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    ABSTRACT: With the rise of the burden of ischemic heart disease, both clinical and economic evidence show a desperate need to protect the heart against myocardium ischemia-reperfusion injury-related complications following cardiac surgery or percutaneous coronary intervention. However, there is no effective intervention for myocardium ischemia-reperfusion injury as yet. We pretreated mice with 4 daily 2.0 absolute atmosphere (ATA) hyperbaric oxygen, then observed its effects on heart function parameters and infarct size following in situ ischemia-reperfusion. Multiple oxidative and inflammation products were measured in the myocardium. Next, we investigated the expression of heme oxygenase 1 (HO-1), phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase (Akt) pathway, and NF-E2-related factor 2 (Nrf2) in the presence of myocardium ischemia-reperfusion injury, hyperbaric oxygen preconditioning, and their inhibitors and their effects on heart function parameters. Hyperbaric oxygen preconditioning ameliorated the cardiac function and histological alterations induced by myocardium ischemia-reperfusion injury, decreased oxidative products and proinflammatory cytokine. Hyperbaric oxygen preconditioning increased expression of HO-1, which was suppressed by PI3K inhibitor LY294002, Nrf2 knockout, and Akt inhibitor triciribine. The expression of Nrf2 was enhanced by hyperbaric oxygen preconditioning, but decreased by LY294002 and triciribine. The Akt was also activated by hyperbaric oxygen preconditioning but suppressed by LY294002. The hemodynamic assays showed that cardiac function was suppressed by LY294002, Nrf2 knockout, and triciribine. These data present a novel signaling mechanism by which hyperbaric oxygen preconditioning protects myocardium ischemia-reperfusion injury via PI3K/Akt/Nrf2-dependent antioxidant defensive system. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 01/2015; DOI:10.1177/1074248414568196
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    ABSTRACT: Atorvastatin has been demonstrated to reduce the incidence of postoperative atrial fibrillation (POAF) in patients undergoing cardiac surgery, but its effect on isolated heart valve surgery is unknown. In a randomized, double-blinded, placebo-controlled trial, 58 patients who underwent isolated heart valve surgery supported by on-pump cardiopulmonary bypass were randomly assigned to receive either placebo (n = 29) or 40 mg of atorvastatin once daily starting 3 days preoperatively and continuing within 5 days postoperatively (n = 29). A continuous monitoring tool and an electrocardiographic Holter monitoring were used for detecting the POAF (Clinical Trial Registration:; Unique Identifier: NTC02084069). The patients' median age was 49 years, and 67% were female. In all, 6 (21%) and 13 (45%) cases of POAF were observed in the atorvastatin and placebo groups, respectively (P = .050). The duration of AF before re-establishment of sinus rhythm was significantly lower in the atorvastatin group than in the placebo group (median of 70 vs 132 minutes, P = .026). The lengths of intensive care unit and hospital stay were comparable between the groups. The increase in postoperative white blood cell count was significantly lower in the atorvastatin group than in the placebo group (median of 1.5 vs 2.3 × 10(3)/µL, respectively, P = .019). After adjustment, the atorvastatin treatment was associated with a decrease in the risk of developing POAF (odds ratio 0.122, 95% confidence interval 0.027-0.548, P = .006). Perioperative treatment with 40 mg of atorvastatin is useful to decrease the incidence of POAF in the statin-naive patients undergoing isolated heart valve surgery. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 12/2014; DOI:10.1177/1074248414564869
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    ABSTRACT: To investigate whether slight variations in core temperature prior to cardiac arrest (CA) influence short-term outcomes and mitochondrial functions. Three groups of New Zealand White rabbits (n = 12/group) were submitted to 15 minutes of CA at 38°C (T-38 group), 39°C (T-39), or 40°C (T 40) and 120 minutes of reperfusion. A Sham-operated group (n = 6) underwent only surgery. Restoration of spontaneous circulation (ROSC), survival, hemodynamics, and pupillary reactivity were recorded. Animals surviving to the end of the observation period were euthanized to assess fresh brain and heart mitochondrial functions (permeability transition and oxidative phosphorylation). Markers of brain and heart damages were also measured. The duration of asphyxia required to induce CA was significantly lower in the T-40 group when compared to the T-38 group (P < .05). The rate of ROSC was >80% in all groups (P = nonsignificant [ns]). Survival significantly differed among the T-38, T-39, and T-40 groups: 10 (83%) of 12, 7 (58%) of 12, and 4 (33%) of 12, respectively (log-rank test, P = .027). At the end of the protocol, none of the animals in the T-40 group had pupillary reflexes compared to 8 (67%) of 12 in the T-38 group (P < .05). Troponin and protein S100B were significantly higher in the T-40 versus T-38 group (P < .05). Cardiac arrest significantly impaired both inner mitochondrial membrane integrity and oxidative phosphorylation in all groups. Brain mitochondria disorders were significantly more severe in the T-40 group compared to the T-38 group (P < .05). Small changes in body temperature prior to asphyxial CA significantly influence brain mitochondrial functions and short-term outcomes in rabbits. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 12/2014; DOI:10.1177/1074248414562911
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    ABSTRACT: Antiplatelet (AP) therapy is well established for the secondary prevention of acute coronary events. However, patients may discontinue treatment, often owing to gastrointestinal (GI) complications, leaving them at elevated risk of recurrent cardiovascular events. This descriptive retrospective study assessed trends in prescription of AP agents and coprescription of gastroprotective therapy, after an acute coronary event. Discontinuation of AP therapy within 2 years of an event and factors predicting discontinuation were investigated. The study was conducted in a UK primary care setting from 2000 to 2008; a total of 27 351 patients aged 50 to 84 years were included in the analysis. Main outcome measures were exposures to low-dose acetylsalicylic acid (ASA), clopidogrel, and proton pump inhibitors (PPIs). At 90 days after an acute coronary event, 85.9% of patients had been prescribed some form of AP therapy and 33.6% of patients who were issued at least 1 ASA prescription in this period were also issued a PPI prescription. The use of dual antiplatelet therapy (DAT) 90 days after an event increased from 2% in 2000 to over 50% in 2008. An estimated 15.1% of patients on ASA monotherapy and 37.5% on DAT discontinued treatment within 1 year. A bleeding event during follow-up, including upper GI bleeding or hemorrhagic stroke, was the strongest predictor of discontinuation. Although most patients were prescribed AP therapy in the 90 days following an acute coronary event, a substantial proportion discontinued DAT or ASA monotherapy within 1 year. It is essential that physicians consider strategies to reduce the risk of discontinuation of AP therapy. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 12/2014; DOI:10.1177/1074248414562910
  • Journal of Cardiovascular Pharmacology and Therapeutics 12/2014; DOI:10.1177/1074248414557890
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    ABSTRACT: This paper summarizes the pharmacologic properties of vasoactive medications used in the treatment of shock, including the inotropes and vasopressors. The clinical application of these therapies is discussed and recent studies describing their use and associated outcomes are also reported. Comprehension of hemodynamic principles and adrenergic and non-adrenergic receptor mechanisms are salient to the appropriate therapeutic utility of vasoactive medications for shock. Vasoactive medications can be classified based on their direct effects on vascular tone (vasoconstriction or vasodilation) and on the heart (presence or absence of positive inotropic effects). This classification highlights key similarities and differences with respect to pharmacology and hemodynamic effects. Vasopressors include pure vasoconstrictors (phenylephrine and vasopressin) and inoconstrictors (dopamine, norepinephrine, and epinephrine). Each of these medications acts as vasopressors to increase mean arterial pressure by augmenting vascular tone. Inotropes include inodilators (dobutamine and milrinone) and the aforementioned inoconstrictors. These medications act as inotropes by enhancing cardiac output through enhanced contractility. The inodilators also reduce afterload from systemic vasodilation. The relative hemodynamic effect of each agent varies depending on the dose administered, but is particularly apparent with dopamine. Recent large-scale clinical trials have evaluated vasopressors and determined that norepinephrine may be preferred as a first-line therapy for a broad range of shock states, most notably septic shock. Consequently, careful selection of vasoactive medications based on desired pharmacologic effects that are matched to the patient's underlying pathophysiology of shock may optimize hemodynamics while reducing the potential for adverse effects. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014; DOI:10.1177/1074248414559838
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    ABSTRACT: The objective of this study is to examine whether carbon monoxide-releasing molecules (CORMs) can decrease the generation of excessive reactive oxygen species (ROS) in cardiac mitochondria, thereby protecting against postresuscitation myocardial injury and cardiac mitochondrial dysfunction after resuscitation in a rat model of ventricular fibrillation (VF), and further investigated the underlying mechanism. Rats suffered 8 minutes of untreated VF and resuscitation and were randomized into the control group with vehicle infusion and the CORM group with CO-releasing molecule 2 (CORM2) treatment. Animals in the Sham group were instrumented without induced VF and resuscitation. Effects of CORM2 on cardiac function, myocardial oxidative stress, cardiac mitochondrial function, and mitochondrial ROS generation were assessed. Moreover, to further evaluate the direct effect of CORM2 on cardiac mitochondria isolated from resuscitated rats, we measured mitochondrial function and ROS generation when isolated cardiac mitochondria were directly incubated with different concentrations of (CORM2). Compared with the Sham group, the control and CORM groups demonstrated impaired cardiac function, increased myocardial injury, and aggravated mitochondrial damage. CORM2 improved cardiac performance and attenuated myocardial damage and oxidative stress in resuscitated rats. Additionally, animals with CORM2 treatment showed the decreased generation of cardiac mitochondrial ROS, alleviated mitochondrial injury, and preserved mitochondrial function and complex activities when compared with the control group. In isolated cardiac mitochondria incubated with CORM2, low concentrations of CORM2 (20 μmol/L) mildly uncoupled mitochondrial respiration, leading to reduced mitochondrial ROS production. In contrast, high concentrations of CORM2 (60 μmol/L) resulted in the reverse effect presumably due to its excessive uncoupling action. These findings suggest that CORM2 attenuates oxidative stress of the heart and improves cardiac function after resuscitation. The mechanism was probably that CO, the product of CORM2, reduces the production of cardiac mitochondrial ROS and thereby attenuates mitochondrial injury and dysfunction during the postresuscitation period, due to the transient uncoupling of mitochondrial respiration. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014; DOI:10.1177/1074248414559837
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    ABSTRACT: Antibody-coated stents to capture circulating endothelial progenitor cells (EPCs) for re-endothelialization appear to be a novel therapeutic option for the treatment of atherosclerotic disease. Hydroxybutyl chitosan (HBC), a linear polysaccharide made from shrimps and other crustacean shells, is biocompatible, nontoxic, and hydrophilic, making it ideal for biomedical applications. In this study, HBC was explored for the immobilization of anti-CD133 antibodies. We demonstrated that CD133 antibodies mediated by HBC were successfully coated on cobalt-chromium alloy discs and metal stents. The coating was homogeneous and smooth as shown by electronic microscopy analysis. Balloon expansion of coated stents did not cause cracking or peeling. The HBC discs promoted CD133+ EPCs and human umbilical vein endothelial cell growth in vitro. The CD133 antibody-coated but not bare discs bound CD133+ EPCs in vitro. Implantation of CD133 antibody-coated stents significantly inhibited intimal hyperplasia and reduced restenosis compared with implantation of bare stents in a porcine model of atherosclerosis. These findings suggest HBC is a valuable anchoring agent that can be applied for bioactive coating of stents and that CD133 antibody-coated stents might be a potential therapeutic alternative for the treatment of atherosclerotic disease. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014; DOI:10.1177/1074248414558518
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    ABSTRACT: Recent clinical studies have reported the potential benefit of an early mineralocorticoid receptor (MR) blockade with potassium canrenoate (PC) on ventricular arrhythmias (VAs) occurrence in patients experiencing an ST-segment elevation myocardial infarction (STEMI). However, most of the electrophysiological properties of PC demonstrated to date have been investigated in normoxic conditions, and therefore, in vitro experiments during an acute myocardial ischemia-reperfusion were lacking.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014; DOI:10.1177/1074248414557036
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    ABSTRACT: This study investigated the effect of 6-week supplementation of a probiotic strain Lactobacillus salivarius UBL S22 with or without prebiotic fructo-oligosaccharide (FOS) on serum lipid profiles, immune responses, insulin sensitivity, and gut lactobacilli in 45 healthy young individuals. The patients were divided into 3 groups (15/group), that is, placebo, probiotic, and synbiotic. After 6 weeks, a significant reduction (P < .05) in total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides and increase in high-density lipoprotein cholesterol was observed in the probiotic as well as in the synbiotic group when compared to placebo; however, the results of total cholesterol and LDL-cholesterol were more pronounced in the synbiotic group. Similarly, when compared to the placebo group, the serum concentrations of inflammatory markers such as high sensitivity C-reactive protein, interleukin (IL) 6, IL-1β, and tumor necrosis factor α were significantly (P < .05) reduced in both the experimental groups, but again the reduction in the synbiotic group was more pronounced. Also, an increase (P < .05) in the fecal counts of total lactobacilli and a decrease (P < .05) in coliforms and Escherichia coli was observed in both the experimental groups after 6 weeks of ingestion. Overall, the combination of L salivarius with FOS was observed to be more beneficial than L salivarius alone, thereby advocating that such synbiotic combinations could be therapeutically exploited for improved health and quality of life.
    Journal of Cardiovascular Pharmacology and Therapeutics 10/2014; DOI:10.1177/1074248414555004