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Effects of continuous intermedin infusion on blood pressure and hemodynamic function in spontaneously hypertensive rats

Ying YUAN ; Xi WANG ; Qiang ZENG ; Hongmei WU ; Yongfen QI ; Chaoshu TANG

Journal of Geriatric Cardiology.2012;09(1):17-27. doi:10.3724/SP.J.1263.2012.00017

Objective To examine the effects of exogenously administered intermedin (IMD,adrenomedullin-2) on arterial blood pressure,cardiac function and the cardiovascular IMD receptor system in spontaneously hypertensive rats (SHRs) as well as to investigate the associated mechanisms.Methods Thirteen week-old male rats were divided in Wistar Kyoto (WKY) group (n =12),SHR group (n =12),IMD group (SHRs infused with IMD 1-47 500 ng/kg per hour,n =12),and ADM group (SHRs infused with adrenomedullin 500 ng/kg per hour,n =12).Results A two-week continuous administration of low dose IMD 1-47 via mini-osmotic pumps markedly reduced blood pressure,the maximal rates of increase and decrease of left-ventricle pressure development (LV ± dp/dtmax),left ventricular systolic pressure and heart rate in SHRs.Furthermore,IMD also inhibited protein over-expression of cardiovascular IMD receptors,myocardial Receptor Activity-Modifying Proteins (RAMP1 and RAMP2),aortic RAMP1,RAMP2,RAMP3,and calcitonin receptor-like receptor (CRLR);suppressed up-regulation of aortic RAMP1,RAMP2,RAMP3 and CRLR gene expression; and markedly elevated the mRNA abundance of myocardial atrial natriuretic peptide (ANP) and myocardial brain natriuretic peptide (BNP).Additionally,IMD 1-47 administration in SHRs increased aortic cAMP concentration and reduced myocardial cAMP concentration.Conclusion These findings support the speculation that IMD,as a cardiovascular active peptide,is involved in blood pressure reduction and cardiac function amelioration during hypertension.The mechanism underlying this effect may involve IMD binding of a receptor complex formed by RAMPs and CRLR,and consequential regulation of cAMP levels and other cardiovascular active factors,such as ANP and BNP.

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Effects of antioxidants on homocysteine thiolactone-induced apoptosis in human umbilical vein endothelial cells

Weijun GU ; Juming LU ; Guoqing YANG ; Qinghua GUO ; Baoan WANG ; Yiming MU ; Changyu PAN

Journal of Geriatric Cardiology.2006;3(2):107-111.

Background and objectives Hyperhomocysteinemia is an independent risk factor for cardiovascular disease. Homocysteine thiolactone (HcyT), one of the homocysteine metabolites in vivo, is toxic both in vivo and in vitro. The aim of this study was to investigate the effect of HcyT on apoptotic damage in human umbilical vein endothelial cells (HUVECs) and the role of antioxidants in the reduction of HcyT-induced apoptosis. Methods HUVECs were cultured in DMEM supplemented with 20% heat inactivated fetal bovine serum cell cultures were maintained in a humidified 5% CO2 atmosphere at 37 ℃. Cytotoxicity was determined by MTT assay,which consists of hypodiploid cells with propidium iodide labeling and intracellular reactive oxygen species levels using 2',7'-dichlorofluorescein diacetate as the probe by flow cytometry. Results HcyT (250-2000μM) induced HUVECs apoptosis in a time- and concentration-dependent manner. Reactive oxygen species levels rose in response to increasing HcyT concentrations at 24-h incubation.The reduction of cell apoptosis by N-acetylcysteine, vitamin E, or pyrrolidine dithiocarbamate, occurred simultaneously with a significant decrease in intracellular reactive oxygen species levels. Conclusion HcyT exerts its cytotoxic effects on endothelial cells through an apoptotic mechanism involving cellular reactive oxygen species production. The capacity of N-acetylcysteine, vitamin E, and pyrrolidine dithiocarbamate to scavenge HcyT-induced cellular reactive oxygen species correlates well with their efficiency to protect against HcyT-promoted apoptotic damage. The protective effect of pyrrolidine dithiocarbamate on cell apoptosis indicates HcyT-generated hydrogen peroxide may provoke cell apoptosis via activating nuclear factor-kappa binding protein.

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Effects of sea anemone toxin anthopleurin-Q on potassium currents in rats and guinea pig ventricular myocytes

Yan HUANG ; Yang LI ; Hasimu BUAIJIAER ; Juan SUN ; Ping FAN ; Jianguo SONG ; Yuemei HOU ; Mingjiang LI ; Salim MOHAMED ; Emmy OKELLO

Journal of Geriatric Cardiology.2008;5(4):243-247.

To investigate the effect of sea anemone toxin anthopleurin-Q (AP-Q) on potassium currents in isolated rats and guinea pig ventricular myocytes.Methods The ventricular cells of guinea pigs and SD rats were obtained by enzymatic dissociation method.Whole cell patch clamp technique was used to record potassium currents (Ito,IK,and IK1).Results AP-Q 3-100 nmol/L increased Ito in a concentration-dependent manner,with an EC50 value of 12.7 nmol/L.At a potential of +50mV,AP-Q 10nmol/L increased Ito from (13.3±3.4) pA pF-1 to (19.46±4.3) pA pF-1.AP-Q 0.1-100 nmol/L increased IK and IK tail in a concentration-dependent manner with EC50 values of 4.7 nmol/L and 5.0 nmol/L,respectively.AP-Q 1 pmol/L-100 nmol/L increased IK1 in dose-dependent manner,with an EC50 of 0.2 nmol/L.Conclusions The effect of AP-Q on Ito,IK and IK1 may partly explain its mechanism in shortening APD and increasing RP.(J Geriatr Cardiol 2008;5:243-247)

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In situ observation of surface structures of cardiovascular endothelial cells with atomic force microscope

Tong YIN ; Jin LUO ; Yamin MA ; Xiaolong JI ; Yusheng ZHAO ; Shiwen WANG

Journal of Geriatric Cardiology.2009;6(3):178-181.

Objective To observe the surface structures of cardiovascular endothelial cells in situ with atomic force microscope (AFM). Methods Fresh aorta and aortic valve were dissected from 10 healthy male New Zealand white rabbits. Before fixed in 1% formaldehyde, the fresh tissues were washed in the buffer phosphate solution. Under general microscope, the fixed aorta or valve was spread on the double side stick tape which had already been stuck on the glass slide. The intima of aorta or the aorta side of valve was towards upside. Then the specimen was dried under 37 degrees centigrade in an attemperator and was washed with pure water. After dried again, the specimen was loaded on the platform ofNanoScope llla AFM and was scanned in tapping mode with the scanning speed of 0.5 HZ. Results The surface structures of endothelial cell on the fixed and dried tissue could be obsserved clearly in situ with AFM. Aortic endothclial cells were large, branched and arranged sparsely and parallel to the direction of blood flow, whereas endothelial cells on aorta valve surface were small, less branched and arranged intensively and vertical to the direction of blood flow. When the scanning range was dwindled, granular ultra-structures could be observed on the surface of endothelial cells, and, as the scanning range was dwindled further, fissure and convolution could be seen on the surface of granules from aortic endothelial cells. Centre cavity and surrounding swelling volcano-like structure could be seen on the surface of granules from endothelial cells of aortic valve. Conclusions It's feasible to observe the surface ultra-structures of cardiovascular endothelial cells in situ with AFM and morphological information provided by A FM might be of clinical value in future histopathological diagnosis.

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Age-associated alternations in cardiac β-adrenergic receptor signaling

Jing MA ; Shiwen WANG ; Ruiping XIAO

Journal of Geriatric Cardiology.2005;2(4):254-257.

During aging, cardiac contractile response to β-AR stimulation is decreased in humans and animal models. Recent studies demonstrate that the positive inotropic effects of both β1-AR and β2-AR stimulation are significantly decreased with aging.This is accompanied by decreases in both β-AR subtype densities and a reduction in membrane adenylyl cyclase activity. However,neither G protein-coupled receptor kinases (GRKs) nor inhibitory G proteins (Gi) appears to contribute to the age-associated reduction in the β-AR modulation of contraction. Thus, while both aging and chronic heart failure exhibit a diminution in cardiac β-AR responsiveness, only heart failure exhibits increased GRK-mediated desensitization ofβ-Ars and an upregulation of Gi proteins.

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The distribution of 10-year cardiovascular risk in Chinese adults: analysis of the China Health Examination Database (CHED) 2008

Liuxin WU ; Qiang ZEN ; Dongchang QIANG

Journal of Geriatric Cardiology.2010;07(3):131-137.

Objective Global cardiovascular risk assessment has been incorporated into current Chinese guidelines for the management of hypertension and hypercholesterolemia. The aim of our study is to determine the distribution of 10-year risk for ischemic cardiovascular disease (ICVD) among middle-aged Chinese adults, and to evaluate the usefulness of global risk assessment tools in the primary prevention of ICVD in Chinese population.Methods Simplified prediction tools derived from the USA-PRC Collaborative Study of Cardiovascular Epidemiology cohort were applied to the Chinese Health Examination Database (CHED) 2008. 10-year risk for ICVD was estimated in 461 157 ICVD-free subjects (264 432 male and 196 725 female) aged 35 to 59 years. Results Among the male subjects, 82.4% had a 10-year risk for ICVD of <5%, 14.4% of 5% to 12.1 % and 3.4 of≥12.2%, and in female subjects, 86.7% had a 10-year risk for ICVD of <5%, 12.1% of 5% to 12.0% and 1.2% of ≥12.1 %. All subjects with predicted high level ICVD risk (≥ 12.2% in male or ≥ 12.1% in female) had either remarkably elevated (≥160 tnmHg) blood pressure, significantly increased (≥6.22 mml/L) total serum cholesterol or diabetes.Conclusion Using the currently recommended prediction tools, only very small proportions of middle-aged Chinese men and women who were free of ICVD would be classified into high level risk group. These prediction tools are unlikely to help for the medical intervention decision making in Chinese adult patients with hypertension and/or hypercholesterolemia.

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High glucose augments stress-induced apoptosis in endothelial cells

Wenwen ZHONG ; Yang LIU ; Hui TIAN

Journal of Geriatric Cardiology.2009;6(2):102-107.

Hyperglycemia has been identified as one of the important factors involved in the microvascular complications of diabetes, and has been related to increased cardiovascular mortality. Endothelial damage and dysfunction result from diabetes; therefore, the aim of this study was to determine the response of endothelial cells to stressful stimuli, modelled in normal and high glucose concentrations in vitro. Eahy 926 endothelial cells were cultured in 5 mmol/L or 30 mmol/L glucose conditions for a 24 hour period and oxidative stress was induced by exposure to hydrogen peroxide (H2O2) or tumour necrosis factor- α (TNF- α ), following which the protective effect of the glucocorticoid dexamethasone was assessed. Apoptosis, necrosis and cell viability were determined using an ELISA for DNA fragmentation, an enzymatic lactate dehydrogenase assay and an MTT assay, respectively. High glucose significantly increased the susceptibility of Eahy 926 cells to apoptosis in the presence of 500 μmol/L H2O2, above that induced in normal glucose (P<0.02). A reduction of H2O2- and TNF- α -induced apoptosis occurred in both high and low glucose after treatment with dexametha-sone (P<0.05). Conclusion high glucose is effective in significantly augmenting stress caused by H2O2, but not in causing stress alone. These findings suggest a mechanism by which short term hyperglycemia may facilitate and augment endothelial damage.

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Protective effects of trimetazidine against vascular endothelial cell injury induced by oxidation

Shenghu HE ; Fengdi YAN ; Jing ZHAN ; Jianfeng YAN ; Bin YUAN ; Shu CHEN ; Yong XIE

Journal of Geriatric Cardiology.2008;5(4):248-251.

To explore the protective effects of trimetazidine on vascular endothelial cells injury induced by hydrogen peroxide (H2O2) and its pharmacological mechanisms of anti-oxidation.Methods Human umbilical vein endothelial cells (HUVECs) were injured by H2O2.Next,the cells were treated with three different concentrations of trimetazidine (1 μmol/L,10 μmol/L,100μmol/L,respectively).The viability of cells was detected by methyl thiazoeyl tetrazolium (MTT) assay.In addition,malondialdehyde (MDA)contents,superoxide dismutase (SOD) and secretion of NO were measured.Results Trimetazidine could enhance the viability of the injured HUVECs induced by oxidation,decrease the level of MDA,enhance the SOD activity,and increase the secretion of nitrogen monoxide.These effects were in a certain dose-dependent manner and the difference was significant among the three concentrations (P＜0.05).Conclusions Our results suggest that trimctazidine may protect lipid peroxidation and prevent oxidation-induced cellular dysfunction of HUVECs (J Geriatr Cardiol 2008;5:248-251)

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Antiarrhythmic peptide AAPl0 prevents ventricular arrhythmia in rabbit LQT2 model

Bodi CHEN ; Xiaoqing QUAN ; Cuntai ZHANG ; Jiagao LU ; Rong BAI ; Nian LIU ; Yanfei RUAN ; Jun KE ; Jin MA ; Liandong LI ; Lei RUAN

Journal of Geriatric Cardiology.2008;5(3):164-168.

Background and Objective Increased transmural dispersion of repolarization (TDR) has been shown to contribute toinitiation and maintenance of ventricular arrhythmia in long QT syndromes(LQTS).Intercellular uncoupling through gap junctions isan important mechanism for maintaining TDR in both intact and diseased heart.The present study was to test the hypothesis thatimproving gap junction communication reduces TDR and prevents ventricular arrhythmia in rabbit LQT2 model.Methods Anarterially perfused rabbit left ventricular preparation and E-403 (0.5μmol/L)were used to establish a model of LQT2.Preparationswere randomly assigned to control(n=10),AAP-100nmol/L(n=10),AAP-500nM(n=10)groups.Transmural ECG as well as actionpotentials from both endocardium and epieardium was simultaneously recorded. Resuits In LQT2 model.presence of 500nmol/LAAP10 reduced endocardial action potential and TDR and prevented ventricular arrhythmia comparing with the control and AAP 100nmol/Lgroups(P＜0.05).Conclusions The presence of 500 nmol/LAAP10 reduces TDR and prevents ventricular arrhythmia in rabbitventricular model of LOT2.This study suggests a possible role of GJs in TDR in rabbit LQT2 model and indicates a new clinicalapproach to the management of LQTS.

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Subclavian artery angioplasty in elderly patients with coronary-subclavian steal syndrome: preliminary comparison between a modified brachial technique and the standard femoral approach

Rigatelli GIANLUCA ; Cardaioli PAOLO ; Giordan MASSIMO ; Panin STEFANO ; Oliva LAURA ; Milan TRANQUILLO ; Roncon LORIS

Journal of Geriatric Cardiology.2007;4(2):73-76.

Background and Objective Elderly patients who have been submitted to coronary bypass grafting with the left internal mammary artery (LIMA) may develop a coronary-subclavian steal syndrome because of a left subclavian artery (LSA) stenosis. Usually stenting of LSA is performed by the standard femoral route with guiding catheter technique, but this technique can be particularly difficult in elderly patients who often have iliac-femoral kinking and aortic tortuosity. We compared a new ad hoc brachial artery approach technique with the standard guiding catheter technique through the femoral access. Methods Between January 2005 and September 2006, four patients underwent LSA stenting using the left brachial artery access obtained with a 6F or 7F 45-cm-long valved anti-kinking sheath as the Super Arrow Flex sheath (Arrow International, PA, USA). The sheath was positioned just before the LIMA graft ostium and a 0.035 inch 260-cm-long Storq guidewire (Cordis Inc., Johnson & Johnson, Warren, NJ) was advanced across the lesion to the descending aorta. A balloon-expandable Genesis (Cordis Inc., Johnson & Johnson, Warren, NJ) endovascular stent was easily deployed, and the correct position was checked by direct contrast injection through the long sheath. This small group of patients has been compared to a group of 5 age-matched patients with coronary steal syndrome in whom the procedure has been performed with standard technique including femoral approach and guide catheter. Results The procedure was successful in all patients; vertebral and LIMA ostia remained patent in all cases. In the control group, cannulation of the subclavian artery was difficult in two cases, while one patient developed a groin hematoma. Mean pretreatment gradient was 32 mm Hg with a range of 25 to 40 mm Hg (34 mmHg, range 26-43, in the control group, P=0.87) and fell to 2 mm Hg with a range of 0 to 4 mm Hg (3.1 mmHg, range 0 to 5, P=0.89) posttreatment. Mean contrast dose was 60±16 ml (138±26 ml in the control group, P＞0.01), whereas mean fluoroscopy and procedural time were 5.7±1.6 minutes (10.8±1.0 minutes in the control group, P＞0.01) and 15.7±6.3 minutes (28±7.1 minutes in the control group, P＞0.01). At a mean follow-up of 10±3.2 months all patients are alive and free from angina and residual induced ischemia. Conclusions Our brief study suggested that brachial artery access be considered the optimal route to treat coronary-subclavian steal syndrome in elderly patients because of clear advantages; these included no manipulation of catheter to cannulate the artery, perfect coaxial position of the catheter at the site of LSA stenosis, clear visualization of the LIMA and vertebral ostia, and easy access to these vessels in case of plaque shifting or embolic protection device deployment.

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