Action Potentials ; drug effects ; physiology ; Animals ; Female ; Guinea Pigs ; Heart Ventricles ; drug effects ; Papillary Muscles ; drug effects ; physiology ; Progesterone ; pharmacology

Action Potentials ; drug effects ; Animals ; Estradiol ; pharmacology ; Female ; Guinea Pigs ; Heart Ventricles ; cytology ; Myocardial Contraction ; drug effects ; Papillary Muscles ; drug effects ; physiology ; Progesterone ; pharmacology

The effects of vanadate on cellular Ca2+ movements across the sarcolemma of cardiac muscle cells were investigated by measuring the intracellular and extracellular Ca2+ activities of guinea pig papillary muscle with Ca2+-selective electrodes. During the rest period following a steady-state of 2 contractions per second the extracellular Ca2+ concentration was increased over the basal level within a minute. During the rest period Ca2+ was transported across the sarcolemma into the extracellular space. Vanadate decreased the change in extracellular Ca2+ concentration during the rest period implying that the Ca2+ efflux across the sarcolemma was decreased by vanadate. Vanadate increased intracellular Ca2+ activities significantly (from 1.9 X 10(-7) M to 10(-6)M) resulting in an increase in resting tension. These results suggest that vanadate decreases Ca2+ efflux from the cells into the extracellular space by blocking Ca2+ transport across the sarcolemma, possibly blocking the Na+-Ca2+ exchange transport.
Animal ; Calcium/metabolism* ; Female ; Guinea Pigs ; Ion Channels/drug effects* ; Male ; Membrane Potentials/drug effects ; Papillary Muscles/drug effects* ; Vanadates ; Vanadium/pharmacology*

The removal of Ca2+ from the cardioplegic solutions could cause the danger of inducing a "calcium paradox" during reperfusion. Since intracellular Ca2+ activities are coupled to Na+ activities via Na(+)-Ca2+ exchange, an increase in intracellular Na+ activities during the cardioplegia could cause an abrupt Ca2+ influx when reperfused. To study the effects of Na+ and Ca2+ concentrations in cardioplegic solutions on intracellular Ca2+ activities during the cardioplegia and subsequent recovery period, the membrane potential and intracellular Na+ and Ca2+ activities of guinea pig ventricular papillary were measured. 1) A cardioplegia with low Ca2+ cardioplegic solution significantly decreased the overshoot and duration of the first action potential after cardioplegia, but the changes in action potential configuration were minimized after a cardioplegia with Ca2+ concentration adjusted according to the Na(+)-Ca2+ exchange mechanism. 2) Intracellular Na+ activity was continuously decreased during the cardioplegia, and the intracellular Na+ activity 20 minutes after cardioplegia was the highest with low Ca2+ cardioplegic solution. 3) Intracellular Na+ and Ca2+ activities were continuously decreased during the cardioplegia with Ca2+ concentration adjusted according to the Na(+)-Ca2+ exchange mechanism. 4) During a reperfusion of Tyrode solution after cardioplegia intracellular Na+ and Ca2+ activities were increased. Intracellular Ca2+ activity was increased more rapidly than intracellular Na+ activity. 5) The rate of increase in intracellular Ca2+ activity with reperfusion of Tyrode solution was dependent upon intracellular Na+ activity during cardioplegia, in such a way that the higher the intracellular Na+ activity was, the faster the intracellular Ca2+ activity increased. These data suggest that Na(+)-Ca2+ exchange mechanism may play an important role in the regulation of intracellular Ca2+ activity during recovery after cardioplegia.
Animal ; Calcium/*pharmacology ; Cardioplegic Solutions/*pharmacology ; Ions ; *Myocardial Reperfusion ; Osmolar Concentration ; Papillary Muscles/cytology/*drug effects ; Sodium/*pharmacology ; Solutions/pharmacology

The membrane permeability to potassium at a resting state is greater than to any other ions and the maintenance of resting membrane potential is largely dependent on K+ concentration of outside medium (Hodgkin and Horowicz 1959), i.e. an increase of K+ concentration of medium induces a depolarization, vice versa. However, on the contrary to this prediction, in some mammalian heart muscle a reduction of external K+ concentration induces a depolarization of membrane potential rather than a hyperpolarization (Vassalle 1965). In this study it was aimed to elucidate the possible mechanism of spontaneous depolarization induced by low external K+ in canine Purkinje fibers. The membrane potential was constantly recorded while components of cations in the bathing medium were replaced one by one by equimolar sucrose until the low K+ induced depolarization was blocked. The results are summarized as follows; The membrane potential of canine Purkinje fibers was spontaneously depolarized by low external K+, and the magnitude of depolarization was not affected by verapamil TEA, and a partial replacement of external Na+ and Ca2+ with choline chloride. But the membrane potential was hyperpolarized only when the all external cations were substitued with sucrose; and this hyperpolarization was disappeared again by substitution of sucrose with choline chloride. From these results, it may be concluded that the depolarization induced by low external K+ in canine Purkinje fibers is due to the nonspecific increase of membrane permeability to external cations and/or combinations with decreased K+ conductance.
Animal ; Dogs ; Guinea Pigs ; Heart/physiology* ; Membrane Potentials/drug effects* ; Papillary Muscles/physiology ; Potassium/pharmacology* ; Purkinje Fibers/physiology ; Rest

The purpose of this study was to investigate the electrophysiological effects of resveratrol on guinea pig papillary muscles and the underlying mechanism. Action potentials were recorded by using intracellular microelectrode technique. The results obtained are as follows: (1) In normal papillary muscles, resveratrol (30, 60, and 120 micromol/L) shortened the duration of action potential (APD) in a concentration-dependent manner. (2) In partially depolarized papillary muscles, resveratrol (60 micromol/L ) not only shortened APD, but also decreased the amplitude of action potential (APA), overshoot (OS) and maximal rate of depolarization in phase 0 (Vmax). (3) Perfusion with Ca2+-free K-H solution, completely abolished the effects of resveratrol (60 micromol/L) on papillary muscles. (4) Application of potassium channel blocker tetraethylammonium chloride (TEA, 20 mmol/L) did not prevent the effect of resveratrol (60 micromol/L) on action potential. (5) Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a nitric oxide (NO) synthase inhibitor, failed to abolish the effect of resveratrol (60 micromol/L). All these results indicate that the electrophysiological effects of resveratrol on guinea pig papillary muscles are likely due to the reduction of calcium influx, which might not be mediated by NO.
Action Potentials ; drug effects ; Animals ; Calcium Channel Blockers ; pharmacology ; Guinea Pigs ; In Vitro Techniques ; Male ; Microelectrodes ; Papillary Muscles ; drug effects ; physiology ; Stilbenes ; pharmacology

The purpose of this study was to investigate the effects of phytoestrogen genistein (GST) on delayed after depolarization (DAD) and triggered activity (TA) induced by ouabain in guinea pig papillary muscles. Action potentials (APs) were recorded from the guinea pig papillary muscles with standard glass microelectrode technique. The results are as follows: (1) DAD and TA induced by ouabain (1 micromol/L) were markedly inhibited by pretreatment with GST (10, 50, 100 micromol/L) in a concentration-dependent manner. (2) NG-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), an NO synthase inhibitor, failed to affect the above effects of GST. (3) 5 micromol/L 17beta-estradiol (E2) or 10 micromol/L GST alone showed no effects on DAD and TA, whereas GST combined with E(2) at the same doses exerted significant inhibitory effects on DAD and TA. Since GST is known to reduce the calcium influx, it is suggested that GST might have antiarrhythmic effects, possibly by reducing calcium influx. The antiarrhythmic effects of GST may contribute to its cardioprotective action.
Action Potentials ; drug effects ; Animals ; Genistein ; pharmacology ; Guinea Pigs ; Male ; Neuromuscular Depolarizing Agents ; pharmacology ; Ouabain ; pharmacology ; Papillary Muscles ; drug effects ; physiology ; Phytoestrogens ; pharmacology

This study is to evaluate the effects of Shenmai injection on the temporal alterations of action potential (AP), early afterdepolarization (EAD) and delayed afterdepolarization (DAD) in papillary muscles. The action potentials were recorded by a glass electrode. APD at 90% repolarization (APD9 ) was measured, and spontaneous EAD and DAD were observed. The results show APD90 was significantly prolonged in model group compared with sham-operated group, whereas it was remained unchanged in Shenmai injec- tion treatment group and amiodarone group. The spontaneous EADs and DADs were frequently visible in model group. In conclusion, EAD, DAD and trigger activities increase gradually during pathological progression of rat cardiac hypertrophy, and Shenmai injection could improve the action potential change in rat cardiac hypertrophy.
Action Potentials ; drug effects ; Animals ; Blood Pressure ; drug effects ; Cardiomegaly ; physiopathology ; Drug Combinations ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; Heart Ventricles ; drug effects ; physiopathology ; Injections ; Male ; Papillary Muscles ; drug effects ; physiopathology ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the effects of interleukin-2 (IL-2) on the transmembrane potential and contractile force in ventricular papillary muscle of rat and the underlying mechanism.

METHODSThe transmembrane potentials and contractile force were recorded by intracellular glass microelectrode and tension transducer in the isolated rat papillary muscles.

RESULTS(1) IL-2 shortened the action potential duration (APD50 and APD80), while had no effects on resting potential, action potential amplitude and depolarization rate. (2) IL-2 depressed the contractile force of the muscle in dose-dependent manner. IL-2 at concentrations of 0.5, 2.5, 10, 50 and 200 u/ml decreased the developed tension to 94.8% (P < 0.05), 85.8%, 76.3%, 69.3% and 52.5% (P < 0.01), respectively. (3) Pretreatment with L-NAME (10(-4) mol/L) attenuated the negative inotropic effect of IL-2, in which effect of IL-2 at concentrations from 0.5 to 10 u/ml was completely abolished, and the effect of IL-2 at high dose (50 and 200 u/ml) was partly attenuated by L-NAME.

CONCLUSIONIL-2 had inhibitory effects on action potential duration and contractile force of papillary muscle, and its negative inotropic effect was mediated by nitric oxide.

Action Potentials ; drug effects ; Animals ; Heart Ventricles ; drug effects ; Interleukin-2 ; pharmacology ; Male ; Myocardial Contraction ; drug effects ; physiology ; Nitric Oxide ; metabolism ; Papillary Muscles ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the electrophysiological changes of ventricular myocardium of rats with experimental diabetes and the effect of adenosine on its electrophysiology.

METHODSDiabetes was induced in male SD rats, using a single injection of alloxan into tail vein. Untreated animals were used as controls. The electrocardiograms (ECG) were recorded 6 weeks after diabetes was induced. Effects of adenosine on ventricular myocardium in diabetic rats and controls were observed by measuring the transmembrane potentials with conventional glass microelectrodes.

RESULTSQT interval in ECG and action potential duration (APD) at all levels (APD30, APD50, APD70 and APD90) were significantly prolonged in right ventricular papillary muscle 6 week after diabetes was induced. No differences were observed in the resting membrane potential (RP), action potential amplitude (APA) and overshoot (OS) as well as the maximum rate of depolarization (Vmax) between the diabetic rats and control rats. At concentration of 10 approximately 400 micromol/L, ADO had little influence on all transmembrane potential parameters of right ventricular papillary muscle in diabetic rats and controls. At 500 micromol/L, ADO shortened APD30, APD50, APD70 and APD90 of control group, while having no effect on diabetic rats.

CONCLUSIONQT interval in ECG and APD at all levels are significantly prolonged in right ventricular papillary muscle of experimentally induced-diabetic rats.

Action Potentials ; drug effects ; Adenosine ; pharmacology ; Animals ; Anti-Arrhythmia Agents ; pharmacology ; Diabetes Mellitus, Experimental ; physiopathology ; Electrocardiography ; Electrophysiology ; Male ; Papillary Muscles ; physiology ; Rats ; Rats, Sprague-Dawley ; Ventricular Function