Action Potentials ; drug effects ; Animals ; Cadmium ; toxicity ; Guinea Pigs ; Male ; Myocytes, Cardiac ; drug effects ; physiology

AIMTo learn the electrophysiological interference of levofloxacin (LVFX) to heart in guinea pig.

METHODSHigh, moderate and low doses of LVFX were given to the anesthetic guinea pig via i.p., and QT interval span and corrected QT-interval span in the II leading lines of ECG were recorded and analyzed from 5 min to 360 min after the drug administration. Single ventricular myocytes were obtained and impacted by LVFX solution of different concentrations. Then delayed rectifier potassium currents (I(K)) on single cells were recorded with whole-cell patch clamp technique, and compared with control group(without impact of LVFX).

RESULTS(1) After the administration of LVFX, at the dose of 200 mg/kg. QT-interval span was significantly elongated, and the increasing rate is 19.38% +/- 3.15% (P < 0.05). While at the relatively lower doses of 50 mg/kg and 100 mg/kg, the elongation is of low/no significance (P > 0.05). (2) LVFX inhibited I(K) dose-dependently and time-dependently.

CONCLUSIONLVFX might prolong the QT-interval span by the mechanism of inhibiting I(K), which implies a potential risk in clinical application.

Animals ; Guinea Pigs ; Levofloxacin ; Membrane Potentials ; Myocytes, Cardiac ; drug effects ; physiology ; Ofloxacin ; pharmacology ; Patch-Clamp Techniques

Action Potentials ; drug effects ; physiology ; Animals ; Cadmium ; toxicity ; Calcium Channels, L-Type ; physiology ; Myocytes, Cardiac ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley

BACKGROUNDShen song Yang xin (SSYX) is a compound of Chinese medicine with the effect of increasing heart rate (HR). This study aimed to evaluate its electrophysiological properties at heart and cellular levels.

METHODSThe Chinese miniature swines were randomly assigned to two groups, administered with SSYX or placebo for 4 weeks (n = 8 per group). Cardiac electrophysiological study (EPS) was performed before and after drug administration. The guinea pig ventricular myocytes were enzymatically isolated and whole cell voltage-clamp technique was used to evaluate the effect of SSYX on cardiac action potential (AP).

RESULTSSSYX treatment accelerated the HR from (141.8 +/- 36.0) beats per minute to (163.0 +/- 38.0) beats per minute (P = 0.013) without changing the other parameters in surface electrocardiogram. After blockage of the autonomic nervous system with metoprolol and atropin, SSYX had no effect on intrinsic HR (IHR), but decreased corrected sinus node recovery time (CSNRT) and sinus atrium conducting time (SACT). Intra cardiac EPS showed that SSYX significantly decreased the A-H and A-V intervals as well as shortened the atrial (A), atrioventricular node (AVN) and ventricular (V) effective refractory period (ERP). In isolated guinea pig ventricular myocytes, the most obvious effect of SSYX on action potential was a shortening of the action potential duration (APD) without change in shape of action potential. The shortening rates of APD(30), APD(50) and APD(90) were 19.5%, 17.8% and 15.3%, respectively. The resting potential (Em) and the interval between the end of APD(30) and APD(90) did not significantly change.

CONCLUSIONSThe present study demonstrates that SSYX increases the HR and enhances the conducting capacity of the heart in the condition of the intact autonomic nervous system. SSYX homogenously decreases the ERP of the heart and shortens the APD of the myocytes, suggesting its antiarrhythmic effect without proarrhythmia.

Action Potentials ; drug effects ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Female ; Guinea Pigs ; Heart ; drug effects ; physiology ; Heart Rate ; drug effects ; Heart Ventricles ; In Vitro Techniques ; Male ; Myocytes, Cardiac ; drug effects ; physiology ; Sinoatrial Node ; drug effects ; physiology ; Swine ; Swine, Miniature

Action Potentials ; drug effects ; Angiotensin II Type 1 Receptor Blockers ; pharmacology ; Animals ; Biphenyl Compounds ; pharmacology ; Calcium Channels, L-Type ; drug effects ; physiology ; Heart Atria ; cytology ; drug effects ; Myocytes, Cardiac ; drug effects ; physiology ; Potassium Channels ; drug effects ; physiology ; Rabbits ; Tetrazoles ; pharmacology

OBJECTIVETo investigate the mechanism of ATP-sensitive potassium channel (K(ATP)) activator cromakalim (CRK) on action potentials and transient inward current (I(ti)) in isolated guinea pig papillary and ventricular myocytes and to explore the mechanisms of effects of I(ti) and K(ATP) treatment in idiopathic ventricular tachycardia.

METHODSThe whole-cell patch clamp recording technique was used to detect the action potentials and I(ti) and K(ATP) current alterations during the stimulated and triggered activity. Myocytes were isolated from guinea pig ventricle by enzyme digestion. The experiment was divided into four groups: (1) Control; (2) Control + Ouabain; (3) Control + CRK; (4) Control + Ouabain + CRK. (5) Control + Ouabain + CRK + glibenclamide (GLB). The action potential of guinea pig papillary muscles was measured by using standard microelectrode. The parameters in the experiment included the amplitude (APA), resting potentials (RP), action potentials duration (APD), as well as maximum rise of the action potential (Vmax).

RESULTS(1) When the guinea pig ventricular papillary myocytes were pretreated with Ouabain 0.5 micromol/L, APD prolonged significantly, especially APD(20), APD(50), APD(90). Delayed after depolorazion (DAD) and triggered activity were elicited. I(ti) currents and DAD as well as triggered activity increased. I(ti) current was (126.9 +/- 10.8) pA, lagT (1173.0 +/- 70.9) ms (n = 10, P < 0.01). (2) When guinea pig ventricular myocytes were pretreated with CRK (10 micromol/L), APD was shortened and the amplitude of DAD was lowered. The coupling time in CRK group was significantly prolonged compared with Ouabain group (n = 10, P < 0.01). (3) CRK 50 micromol/L pretreatment of the ventricular myocytes led to an increase of K(ATP) up to (342 +/- 89) pA, which was statistically significant as compared with the control group (P < 0.01). ATP-sensitive potassium channel blocker glibenclamide (10 micromol/L) could antagonize the effects of CRK on APD and I(ti) currents.

CONCLUSIONCRK might reduce the toxic effect of Ouabain on cardiomyocytes, shorten APD, terminate DAD and trigger excitation, and have protective effect on cardiomyocytes. The effects of CRK, may be associated with the inhibiting I(ti) current and increasing K(ATP).

Action Potentials ; drug effects ; Animals ; Cromakalim ; pharmacology ; Guinea Pigs ; Heart Ventricles ; drug effects ; Myocytes, Cardiac ; drug effects ; physiology ; Patch-Clamp Techniques ; Potassium Channels, Inwardly Rectifying ; agonists

AIMTo explore the effect and mechanism of interleukin-2 (IL-2) on the rhythm of isolated rat heart and neonatal myocytes.

METHODSCultured neonatal rat cardiomyocytes and isolated perfused rat heart were used.

RESULTS(1) IL-2 (2.5-200 u/ml) reduced the spontaneous beating rate of cultured neonatal rat cardiomyocytes in a dose-dependent manner. (2) IL-2 at 50 u/ml increased both the heart rate and the number of premature ventricular excitation in the isolated heart. (3) Pretreatment with propranolol abolished the effect of 50 u/ml IL-2 on the isolated heart. (4) Heat inactivated IL-2 had no significant effect on the cultured cardiomyocytes and isolated hearts.

CONCLUSIONIL-2 inhibited the auto rhythmic of cultured cardiomyocyte directly while the positive chronotropic and arrhythmogenic effects of IL-2 in the isolated rat heart may be mediated by endogenous catecholamine.

Animals ; Animals, Newborn ; Cells, Cultured ; Heart ; drug effects ; Heart Rate ; drug effects ; In Vitro Techniques ; Interleukin-2 ; pharmacology ; Myocytes, Cardiac ; drug effects ; physiology ; Propranolol ; pharmacology ; Rats ; Rats, Sprague-Dawley

The experiments were carried out on guinea pig isolated ventricular myocytes by using whole-cell patch clamp. The effects of angiotensin II (Ang II) on potassium ion channels of acute ischemic myocytes were observed. Whole-cell patch clamp recordings showed that physiological potassium current, including delayed rectifier potassium current and inward rectifier potassium current were inhibited under the condition of simulated ischemia, and then further inhibited by treatment with Ang II. ATP-sensitive potassium currents were increased under simulated ischemia and were further enhanced by Ang II treatment.
Angiotensin II ; pharmacology ; Animals ; Cells, Cultured ; Female ; Guinea Pigs ; Heart Ventricles ; cytology ; drug effects ; Male ; Myocardial Ischemia ; pathology ; physiopathology ; Myocytes, Cardiac ; drug effects ; Potassium Channels ; drug effects ; physiology

OBJECTIVETo study the effects of glycyrrhetinic acid (GA) on the sodium ion channel currents (I(Na)) of rats' ventricular myocardial cells, and to explore its anti-arrhythmic mechanisms at the ion channel level.

METHODSSingle ventricular myocardial cells was isolated from SD rats. The whole cell patch clamp was used to record the effects of GA on I(Na) of rats' ventricular myocardial cells.

RESULTSGA could inhibit I(Na) of rats' ventricular myocardial cells dose-dependently. GA at 1, 5, and 10 micromol/L decreased I(Na) of rats' ventricular myocardial cells from (-4.26 +/- 0.15) nA to (-3.54 +/- 0.10) nA, (-2.19 +/- 0.09) nA, and (-1.25 +/- 0.08) nA, respectively. GA at 1, 5, and 10 micromol/L inhibited I(Na) by 16.08% +/- 2.3%, 50.82% +/- 3.56%, and 75.98% +/- 5.12%, showing statistical difference when compared with the control group (P < 0.05). GA at 10 micromol/L shifted I(Na) current-voltage curve more positively, but the activation potential and the peak potential were not changed.

CONCLUSIONGA inhibited the I(Na) of rats' ventricular myocardial cells dose-dependently, which was possibly associated with its antiarrhythmia effects.

Animals ; Glycyrrhetinic Acid ; pharmacology ; Heart Ventricles ; cytology ; metabolism ; Male ; Myocytes, Cardiac ; drug effects ; physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Sodium Channels ; drug effects ; physiology

AIM AND METHODSTo observe the effects of Puerarin on K+ channel of isolated ventricular myocyte in guinea pig.

METHODSUsing inside-out configuration of patch-clamp single channel recording technique.

RESULTSPuerarin 20 micromol/L, 40 micromol/L, 80 microml/L could inhibit the open-close rate of K+ channel of isolated ventricular myocyte in guinea pig. At 80 micromol/L, Po was decreased from 0.867 +/- 0.13 to 0.019 +/- 0.01 (n = 5, P < 0.05).

CONCLUSIONPuerarin can inhibit K+ channel of isolated ventricular myocyte in guinea pig. It may be the mechanism of Puerarin against arrhythmias in molecular level.

Animals ; Guinea Pigs ; Heart Ventricles ; cytology ; Isoflavones ; pharmacology ; Myocytes, Cardiac ; drug effects ; physiology ; Patch-Clamp Techniques ; Potassium Channels ; drug effects ; physiology