stilbenes and Arrhythmias--Cardiac

To evaluate the preventive cardioprotective effects of resveratrol and grape products, such as grape juice and red wine, in animal model of cardiac ischemia and reperfusion.. Male Wistar rats orally pretreated for 21-days with resveratrol and grape products were anesthetized and placed on mechanical ventilation to surgically induce cardiac ischemia and reperfusion by obstruction (ischemia) followed by liberation (reperfusion) of blood circulation in left descending coronary artery. These rats were submitted to the electrocardiogram (ECG) analysis to evaluate the effects of pretreatment with resveratrol and grape products on the incidence of ventricular arrhythmias (VA), atrioventricular block (AVB) and lethality (LET) resulting from cardiac ischemia and reperfusion.. It was observed that the incidence of AVB was significantly lower in rats pretreated with resveratrol (25%), grape juice (37.5%) or red wine (12.5%) than in rats treated with saline solution (80%) or ethanol (80%). Similarly, incidence of LET was also significantly lower in rats pretreated with resveratrol (25%), grape juice (25%) or red wine (0%) than in rats treated with saline solution (62.5%) or ethanol (75%).. These results indicate that the cardioprotective response stimulated by resveratrol and grape products prevents the lethal cardiac arrhythmias in animal model of ischemia and reperfusion, supporting the idea that this treatment can be beneficial for prevention of severe cardiac arrhythmias in patients with ischemic heart disease.

Topics: Animals; Arrhythmias, Cardiac; Humans; Ischemia; Male; Rats; Rats, Wistar; Reperfusion; Resveratrol; Stilbenes; Vitis

To investigate whether the phosphatidyl-inositol-3-kinase/protein kinase B(PI3K/Akt)pathway is involved in anti-arrhythmia of resveratrol on ischemia/reperfusion in rat hearts.. The phosphorylated levels of Akt and myocardial Cx43 were significantly enhanced in Res group as compared with I/R group(. Resveratrol could prevent the occurrence of reperfusion arrhythmias by increasing the content and ac-tivity of myocardial Cx43 through the PI3K/Akt signaling pathway.

Topics: Animals; Arrhythmias, Cardiac; Chromones; Male; Morpholines; Myocardial Reperfusion Injury; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Rats; Resveratrol; Signal Transduction; Stilbenes; Ventricular Function, Left

The aim of this study was to assess the effect of combined 1,25-dihydroxyvitamin D (1,25 D) and resveratrol on cardiac arrhythmias, infarct size, and transcription of catalase, thioredoxin-1 and B-cell lymphoma 2 (Bcl-2), following myocardial ischemia-reperfusion (IR) in male rats. Ligation of coronary artery was performed in rats (n = 6 per group) without any treatment (IR group), pretreated with 0.1 μg/kg/day of 1,25 D (1,25 D + IR), 1 mg/kg/day of resveratrol (Res + IR) or a combination (1,25 D + Res + IR) for 14 days. Arrhythmias were analyzed according to the Lambeth conventions, and infarct size was measured by 2,3,5-triphenyl-2H-tetrazolium chloride staining. Expression of prosurvival genes was evaluated by real-time polymerase chain reaction. In the 1,25 D + Res + IR group the mean infarct size was 17.6 ± 3.5 %, which was significantly less than that in the IR, 1,25 D + IR, and Res + IR groups (p < 0.001). Although the single therapy of either 1,25 D or resveratrol did not change the incidence of arrhythmias significantly, a reduction in the number of ventricular ectopic beats was noted in group 1,25 D + Res + IR (179.19 ± 58.87, p < 0.001 vs IR; p < 0.05 vs Res + IR; p < 0.01 vs Vit D + IR). Combination of 1,25 D and resveratrol increased transcription of catalase by 119 ± 37 % (p < 0.001 vs IR, p < 0.01 vs Res + IR, p < 0.001 vs 1,25 D + IR). Our study showed that combination of a non-hypotensive dose of 1,25 D and resveratrol can be a novel and effective strategy for protecting against ischemia.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Arrhythmias, Cardiac; Calcium; Drug Therapy, Combination; Male; Myocardial Infarction; Rats; Rats, Wistar; Real-Time Polymerase Chain Reaction; Reperfusion Injury; Resveratrol; RNA, Messenger; Stilbenes; Vitamin D; Vitamins

Obesity is characterized by dysfunctional white adipose tissue (WAT) that ultimately may lead to metabolic diseases. Calorie restriction (CR) reduces the risk for age and obesity-associated complications. The impact of CR on obesity has been examined with human intervention studies, which showed alterations in circulating adipokines. However, a direct effect of CR on the human adipocyte secretome remains elusive. Therefore, the effect of a 96h low glucose CR on the secretion profile of in vitro cultured mature human SGBS adipocytes was investigated by using proteomics technology. Low-glucose CR decreased the adipocyte triglyceride contents and resulted in an altered secretion profile. Changes in the secretome indicated an improved inflammatory phenotype. In addition, several adipocyte-secreted proteins related to insulin resistance showed a reversed expression after low-glucose CR. Furthermore, 6 novel CR-regulated adipocyte-secreted proteins were identified. Since resveratrol (RSV) mimics CR we compared results from this study with data from our previous RSV study on the SGBS adipocyte secretome. The CR and RSV adipocyte secretomes partly differed from each other, although both treatment strategies lead to secretome changes indicating a less inflammatory phenotype. Furthermore, both treatments induced SIRT1 expression and resulted in a reversed expression of detrimental adipokines associated with metabolic complications.

Topics: Adipocytes; Adipokines; Adipose Tissue, White; Antioxidants; Arrhythmias, Cardiac; Caloric Restriction; Cells, Cultured; Electrophoresis, Gel, Two-Dimensional; Gene Expression Regulation; Genetic Diseases, X-Linked; Gigantism; Glucose; Heart Defects, Congenital; Humans; Insulin Resistance; Intellectual Disability; Molecular Sequence Annotation; Obesity; Proteome; Proteomics; Resveratrol; Sirtuin 1; Stilbenes; Tandem Mass Spectrometry

Increased plasminogen activator inhibitor-1 (PAI-1) levels are associated with a number of pathophysiological complications; among them is obesity. Resveratrol was proposed to improve obesity-related health problems, but the effect of resveratrol on PAI-1 gene expression in obesity is not completely understood. In this study, we used SGBS adipocytes and a model of human adipose tissue inflammation to examine the effects of resveratrol on the production of PAI-1. Treatment of SGBS adipocytes with resveratrol reduced PAI-1 mRNA and protein in a time- and concentration-dependent manner. Further experiments showed that obesity-associated inflammatory conditions lead to the upregulation of PAI-1 gene expression which was antagonized by resveratrol. Although signaling via PI3K, Sirt1, AMPK, ROS, and Nrf2 appeared to play a significant role in the modulation of PAI-1 gene expression under noninflammatory conditions, those signaling components were not involved in mediating the resveratrol effects on PAI-1 production under inflammatory conditions. Instead, we demonstrate that the resveratrol effects on PAI-1 induction under inflammatory conditions were mediated via inhibition of the NF κ B pathway. Together, resveratrol can act as NF κ B inhibitor in adipocytes and thus the subsequently reduced PAI-1 expression in inflamed adipose tissue might provide a new insight towards novel treatment options of obesity.

Topics: Adipocytes; Adipose Tissue; AMP-Activated Protein Kinases; Animals; Arrhythmias, Cardiac; Culture Media, Conditioned; DNA; Down-Regulation; Female; Gene Expression Regulation; Genetic Diseases, X-Linked; Gigantism; Heart Defects, Congenital; Humans; Inflammation; Intellectual Disability; Mice; Models, Biological; NF-E2-Related Factor 2; NF-kappa B; Phosphatidylinositol 3-Kinases; Plasminogen Activator Inhibitor 1; Protein Binding; Reactive Oxygen Species; Resveratrol; RNA, Messenger; Sirtuin 1; Stilbenes; Time Factors; Up-Regulation

To investigate whether resveratrol suppressed oxidative stress-induced arrhythmogenic activity and Ca(2+) overload in ventricular myocytes and to explore the underlying mechanisms.. Hydrogen peroxide (H2O2, 200 μmol/L)) was used to induce oxidative stress in rabbit ventricular myocytes. Cell shortening and calcium transients were simultaneously recorded to detect arrhythmogenic activity and to measure intracellular Ca(2+) ([Ca(2+)]i). Ca(2+)/calmodulin-dependent protein kinases II (CaMKII) activity was measured using a CaMKII kit or Western blotting analysis. Voltage-activated Na(+) and Ca(2+) currents were examined using whole-cell recording in myocytes.. H2O2 markedly prolonged Ca(2+) transient duration (CaTD), and induced early afterdepolarization (EAD)-like and delayed afterdepolarization (DAD)-like arrhythmogenic activity in myocytes paced at 0.16 Hz or 0.5 Hz. Application of resveratrol (30 or 50 μmol/L) dose-dependently suppressed H2O2-induced EAD-like arrhythmogenic activity and attenuated CaTD prolongation. Co-treatment with resveratrol (50 μmol/L) effectively prevented both EAD-like and DAD-like arrhythmogenic activity induced by H2O2. In addition, resveratrol markedly blunted H2O2-induced diastolic [Ca(2+)]i accumulation and prevented the myocytes from developing hypercontracture. In whole-cell recording studies, H2O2 significantly enhanced the late Na(+) current (I(Na,L)) and L-type Ca(2+) current (I(Ca,L)) in myocytes, which were dramatically suppressed or prevented by resveratrol. Furthermore, H2O2-induced ROS production and CaMKII activation were significantly prevented by resveratrol.. Resveratrol protects ventricular myocytes against oxidative stress-induced arrhythmogenic activity and Ca(2+) overload through inhibition of I(Na,L)/I(Ca,L), reduction of ROS generation, and prevention of CaMKII activation.

Topics: Animals; Arrhythmias, Cardiac; Calcium; Cells, Cultured; Heart Ventricles; Male; Myocytes, Cardiac; Oxidative Stress; Rabbits; Reactive Oxygen Species; Resveratrol; Stilbenes

Resveratrol has been demonstrated to be protective in the cardiovascular system. The aim of this study was to assess the effects of resveratrol on hydrogen peroxide (H(2)O(2))-induced increase in late sodium current (I(Na.L)) which augmented the reverse Na(+)-Ca(2+) exchanger current (I(NCX)), and the diastolic intracellular Ca(2+) concentration in ventricular myocytes.. I(Na.L), I(NCX,) L-type Ca(2+) current (I(Ca.L)) and intracellular Ca(2+) properties were determined using whole-cell patch-clamp techniques and dual-excitation fluorescence photomultiplier system (IonOptix), respectively, in rabbit ventricular myocytes.. Resveratrol (10, 20, 40 and 80 µM) decreased I(Na.L) in myocytes both in the absence and presence of H(2)O(2) (300 µM) in a concentration dependent manner. Ranolazine (3-9 µM) and tetrodotoxin (TTX, 4 µM), I(Na.L) inhibitors, decreased I(Na.L) in cardiomyocytes in the presence of 300 µM H(2)O(2). H(2)O(2) (300 µM) increased the reverse I(NCX) and this increase was significantly attenuated by either 20 µM resveratrol or 4 µM ranolazine or 4 µM TTX. In addition, 10 µM resveratrol and 2 µM TTX significantly depressed the increase by 150 µM H(2)O(2) of the diastolic intracellular Ca(2+) fura-2 fluorescence intensity (FFI), fura-fluorescence intensity change (△FFI), maximal velocity of intracellular Ca(2+) transient rise and decay. As expected, 2 µM TTX had no effect on I(Ca.L).. Resveratrol protects the cardiomyocytes by inhibiting the H(2)O(2)-induced augmentation of I(Na.L.)and may contribute to the reduction of ischemia-induced lethal arrhythmias.

Topics: Acetanilides; Animals; Antioxidants; Arrhythmias, Cardiac; Calcium; Diastole; Dose-Response Relationship, Drug; Electrophysiology; Female; Heart Ventricles; Hydrogen Peroxide; Ischemia; Male; Muscle Cells; Patch-Clamp Techniques; Piperazines; Rabbits; Ranolazine; Resveratrol; Sodium; Stilbenes; Temperature; Tetrodotoxin

Oxidative stress and inflammatory response induced by myocardial infarction play important roles in the development of sympathetic neural remodeling. The present study was designed to investigate whether resveratrol can improve sympathetic neural remodeling and hence cause less arrhythmias via its anti-oxidant and anti-inflammatory effects. Male Sprague Dawley rats were randomly assigned to either vehicle or resveratrol (1 mg/kg) treatment for 4 weeks post myocardial infarction. Another group of sham operated rats served as controls. Cardiac electrophysiology examination was performed to evaluate the severity of ventricular arrhythmias. Sympathetic neural remodeling characterized by heterogeneous nerve sprouting and sympathetic hyperinnervation was assessed by immunohistochemistry study. Western blotting and ELISA were used to evaluate inflammatory responses and oxidative stress was also quantified. Resveratrol treatment resulted in less episodes of inducible ventricular arrhythmias which was closely associated with attenuated sympathetic neural remodeling (P<0.001, respectively). Decreased nerve growth factor (NGF) expression was also observed in resveratrol treated rats in the peri-infarct area at 4 weeks after myocardial infarction (P<0.001). Interestingly, beneficial effects of resveratrol were also associated with less inflammatory responses and oxidative stress. Our data indicated that resveratrol can suppress sympathetic neural remodeling process after myocardial infarction via attenuated inflammatory responses and oxidative stress, which in turn leads to less inducibility of ventricular arrhythmias.

Topics: Animals; Anti-Arrhythmia Agents; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Arrhythmias, Cardiac; Biomarkers; Heart Ventricles; Macrophages; Male; Myocardial Infarction; Myocardium; Nerve Growth Factor; Neurons; Oxidative Stress; Random Allocation; Rats; Rats, Sprague-Dawley; Resveratrol; Severity of Illness Index; Stilbenes; Sympathetic Nervous System

Piceatannol is more potent than resveratrol in free radical scavenging in association with antiarrhythmic and cardioprotective activities in ischaemic-reperfused rat hearts. The present study aimed to investigate the antiarrhythmic efficacy and the underlying ionic mechanisms of piceatannol in rat hearts.. Action potentials and membrane currents were recorded by the whole-cell patch clamp techniques. Fluo-3 fluorimetry was used to measure cellular Ca2+ transients. Antiarrhythmic activity was examined from isolated Langendorff-perfused rat hearts.. In rat ventricular cells, piceatannol (3-30 micromol.L(-1)) prolonged the action potential durations (APDs) and decreased the maximal rate of upstroke (V(max)) without altering Ca2+ transients. Piceatannol decreased peak I(Na) and slowed I(Na) inactivation, rather than induced a persistent non-inactivating current, which could be reverted by lidocaine. Resveratrol (100 micromol.L(-1)) decreased peak I(Na) without slowing I(Na) inactivation. The inhibition of peak I(Na) or V(max) was associated with a negative shift of the voltage-dependent steady-state I(Na) inactivation curve without altering the activation threshold. At the concentrations more than 30 micromol.L(-1), piceatannol could inhibit I(Ca,L), I(to), I(Kr), Ca2+ transients and Na+-Ca2+ exchange except I(K1). Piceatannol (1-10 micromol.L(-1)) exerted antiarrhythmic activity in isolated rat hearts subjected to ischaemia-reperfusion injury.. The additional hydroxyl group on resveratrol makes piceatannol possessing more potent in I(Na) inhibition and uniquely slowing I(Na) inactivation, which may contribute to its antiarrhythmic actions at low concentrations less than 10 micromol.L(-1).

Topics: Aconitine; Action Potentials; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Caffeine; Calcium Channel Blockers; Calcium Channels, L-Type; Cell Line; Electric Stimulation; ERG1 Potassium Channel; Ether-A-Go-Go Potassium Channels; Free Radical Scavengers; Humans; In Vitro Techniques; Male; Myocardial Reperfusion Injury; Myocytes, Cardiac; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Resveratrol; Sodium Channel Agonists; Sodium Channel Blockers; Sodium Channels; Stilbenes

Resveratrol (trans-3, 4', 5-trihydroxystilbene), a natural antioxidant derived from grapes, has beneficial effects against coronary heart disease. Its electrophysiological characteristics for antiarrhythmic efficacy are largely unknown; thus, this study aims to explore the resveratrol's antiarrhythmic effects and conduction system in isolated hearts as well as its electrophysiological effects on cardiac myocytes. In the experiment, resveratrol suppressed the ischemia/reperfusion-induced ventricular arrhythmias in Langendorff-perfused rat hearts. In the current clamp study of the experiment, resveratrol prolonged the action potential duration (APD(50) and APD(90)) and suppressed the upstroke velocity of the action potential (V(max)). In the voltage clamp study, resveratrol inhibited sodium inward current (I(Na)) in a concentration-dependent manner and negative-shifted the voltage-dependent inactivation curve. Resveratrol also reduced the calcium inward current (I(Ca), 51.2+/-13.3% at 100 microM). Furthermore, the transient (I(to)) and sustained (I(ss)) outward potassium currents were decreased 60.2+/-5.7% and 42.3+/-5.2% after exposure to resveratrol (100 microM), respectively. The inward rectifier potassium current (I(K1)) was also reduced 24.2+/-7.0% in the presence of resveratrol (100 microM). In the isolated heart perfusion model, resveratrol (100 microM) prolonged AV nodal refractory period, the Wenckebach cycle length and the conduction through AV node and His-Purkinje system. In conclusion, resveratrol increased the cardiac effective refractory period mainly through inhibiting the ionic channels including I(Na), I(to) and I(ss) which could contribute to the conversion of ischemia/reperfusion-induced lethal arrhythmias.

Topics: Action Potentials; Animals; Anti-Arrhythmia Agents; Antioxidants; Arrhythmias, Cardiac; Calcium; Calcium Channels, L-Type; Cells, Cultured; Dose-Response Relationship, Drug; Electrophysiology; Heart Conduction System; In Vitro Techniques; Male; Membrane Potentials; Myocardial Reperfusion Injury; Myocytes, Cardiac; Potassium Channels; Rats; Rats, Sprague-Dawley; Resveratrol; Sodium Channels; Stilbenes; Treatment Outcome; Wine

Resveratrol has been demonstrated to produce a variety of biological actions. Accumulating line of evidence supported the view that resveratrol may exert protective effect on the cardiovascular system. The aim of the study was to assess the antiarrhythmic profile as well as electrophysiological properties of resveratrol. We observe the antiarrhythmic effect of resveratrol on aconitine induced rat arrhythmia, ouabain induced guinea pig arrhythmia, and coronary ligation induced rat arrhythmia animal models. Resveratrol significantly and dose-dependently increased the doses of aconitine and ouabain required to induce the arrhythmia indexes. In coronary ligation induced rat arrhythmia model, resveratrol shortened duration of arrhythmia, decreased incidence of ventricular tachycardia and mortality. Electrophysiological experiment revealed that resveratrol could shorten APD through inhibition of ICa and selective enhancement of IKs without an effect on IKr.

Topics: Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Disease Models, Animal; Dose-Response Relationship, Drug; Fruit; Guinea Pigs; Ion Channel Gating; Muscle Cells; Plant Extracts; Rats; Rats, Wistar; Resveratrol; Stilbenes; Survival Rate; Treatment Outcome; Vitis

We previously showed that resveratrol (3,4',5-trihydroxystilbene) stimulates NO production and is cardioprotective in rat heart subjected to ischemia-reperfusion (I/R rat heart). We now show that in I/R rat heart, inducible nitric oxide synthase (iNOS) expression is markedly induced, while expression of endothelial nitric oxide synthase (eNOS) and nueronal nitric oxide synthase (nNOS) is unchanged. In animals preconditioned with resveratrol (0.5 to 1 mg/kg body wt), I/R-induced iNOS induction is abrogated; however, expression of eNOS and nNOS is greatly upregulated. The protective effects of resveratrol on I/R rat heart include reduced rhythm disturbances, reduced cardiac infarct size, and decreased plasma levels of lactate dehydrogenase (LDH) and creatine kinase (CK). Among these, the reductions in LDH/CK levels and infarct size are NO-dependent as the coadministration of N(omega)-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg body wt) with resveratrol abolishes the resveratrol effect. In contrast, the reductions in the severity of ventricular arrhythmia and mortality rate are not affected by L-NAME coadministration, suggesting that a NO-independent mechanism is involved.

Topics: Animals; Arrhythmias, Cardiac; Blood Pressure; Coronary Disease; Creatine Kinase; Gene Expression; Heart Rate; L-Lactate Dehydrogenase; Models, Animal; Myocardial Infarction; Myocardial Reperfusion Injury; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Rats; Rats, Sprague-Dawley; Resveratrol; RNA, Messenger; Stilbenes

A variety of potentially important macroscopic Cl- currents have been described in the heart. Although the single-channel properties of the cAMP-dependent current (ICl.cAMP) have been well described, the single-channel equivalents of the other forms of cardiac Cl- current remain unknown. Unlike ICl.cAMP, many of these currents show prominent outward rectification in the presence of symmetrical transmembrane Cl- gradients and sensitivity to disulfonic stilbene Cl- transport blockers. We used the patch-clamp technique to search for single Cl- channels in inside-out patches from rabbit atrial cell membranes, under conditions minimizing the chances of observing channels carrying Na+, Ca2+, or K+. Under symmetrical Cl- conditions, single-channel activity was seen in 14 (9%) of 155 patches. Channels showed strong outward rectification and a unitary conductance of 60 +/- 3 picosiemens (mean +/- SEM) at positive voltages. The current-voltage relation was not altered by replacement of cations by the impermeant cation N'-methyl-D-glucamine (NMDG) and shifted as expected for a Cl(-)-selective channel when methanesulfonate was substituted for Cl-. The Cl- transport blockers DIDS (diisothiocyanatostilbene-2,2'-disulfonic acid, 100 mumol/L) and SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid, 1 mmol/L) strongly and reversibly inhibited channel activity when added to the bath and caused channel flickering suggesting open-channel block. Ensemble-average currents showed no time dependence, and the form of the ensemble-average current-voltage relation was similar to that of macroscopic background Cl- current.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Action Potentials; Animals; Arrhythmias, Cardiac; Atrial Function; Calcium Channels; Cell Membrane; Cell Size; Chloride Channels; Electric Conductivity; Heart; Heart Atria; In Vitro Techniques; Myocardium; Potassium Channels; Rabbits; Sodium Channels; Stilbenes

Possible arrhythmogenic effects of the isoproterenol-activated Cl- current were examined in isolated guinea-pig ventricular myocytes under various intra- and extracellular Cl- concentrations. Experiments were carried out with external K+ concentration ([K+]o) decreased to 2 or 3 mM. Under symmetrical concentrations of Cl- in intra- and extra-cellular solutions (ECl = 0 mV), 1 microM isoproterenol (ISP) depolarized resting membrane potential (RMP) by 6.2 +/- 1.1 mV and slowed repolarization with induction of early afterdepolarizations (EADs) in 9 out of 9 cells. EADs appeared at voltages positive to -40 mV, where L-type Ca2+ current is assumed to be activated. When Cl- concentrations were settled near physiological conditions (ECl = -40 - -50 mV), ISP depolarized RMP by 2.8 +/- 0.4 mV and elicited abnormal repolarization with occasional EADs in 6 out of 19 cells. When ECl was set to -80 mV, however, ISP depolarized RMP by only 0.5 +/- 0.5 mV without induction of abnormal activities. Thus, depolarizing effects of ISP and incidence of repolarization abnormalities including EADs were increased as ECl shifted to more positive potential levels. At [K+]o = 4 mM, no abnormal activities were observed when ECl was around -50 mV (0/8), and 6 out of 6 cells showed abnormal activities when ECl was set to 0 mV. ISP-elicited abnormal activities were abolished by 1 mM DNDS (4,4'-dinitrostilbene-2,2'-disulphonic acid), a blocker for Cl- channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Action Potentials; Animals; Arrhythmias, Cardiac; Chloride Channels; Electrophysiology; Guinea Pigs; Heart; In Vitro Techniques; Isoproterenol; Membrane Potentials; Membrane Proteins; Myocardium; Stilbenes