Electrophysiological mechanisms of sophocarpine as a potential antiarrhythmic agent.

Aim: To examine the electrophysiological effects of sophocarpine on action potentials (AP) and ionic currents of cardiac myocytes and to compare some of these effects with those of amiodarone.

Methods: Langendorff perfusion set-up was used in isolated guinea pig heart, and responses to sophocarpine were monitored using electrocardiograph. Conventional microelectrode, voltage clamp technique and perforated patch were employed to record fast response AP (fAP), slow response AP (sAP) and ionic currents in guinea pig papillary muscle or rabbit sinus node cells.

Beta-receptor activation increases sodium current in guinea pig heart.

Aim: To study the influence of beta-receptor activation on sodium channel current and the physiological significance of increased sodium current with regard to the increased cardiac output caused by sympathetic excitation.

Methods: Multiple experimental approaches, including ECG, action potential recording with conventional microelectrodes, whole-cell current measurements, single-channel recordings, and pumping-force measurements, were applied to guinea pig hearts and isolated ventricular myocytes.

Results: Isoprenaline was found to dose-dependently shorten QRS waves, increase the amplitude and the V(max) of action potentials, augment the fast sodium current, and increase the occurrence frequencies and open time constants of the long-open and burst modes of the sodium channel.

Possible arrhythmiogenic mechanism produced by ibuprofen.

Aim: The aim of the present study was to investigate the electrophysiological effect of ibuprofen on the cardiac action potentials (AP) and electrocardiograms (ECG), and to identify its arrhythmiogenic mechanism.

Methods: The intracellular microelectrode recording technique was employed to record the fast- and slowresponse AP in guinea pig papillary muscles. The cardiac responses of ibuprofen were monitored by ECG, both in in vivo and in vitro studies.

Reduced sinoatrial cAMP content plays a role in postnatal heart rate slowing in the rabbit.

1. Decreasing heart rate during development is known to be the result of parasympathetic nervous system maturation that depresses the pacemaker current (If) by acetylcholine (ACh). However, a direct effect of ACh on If has been ruled out and the involvement of other secondary messengers, such as cAMP, was verified in previous studies.

Electrophysiological effect of fluoxetine on Xenopus oocytes heterologously expressing human serotonin transporter.

Aim: To investigate the electrophysiological effect of fluoxetine on serotonin transporter.

Methods: A heterologous expression system was used to introduce human serotonin transporter (hSERT) into Xenopus oocytes. A 2-electrode voltage clamp technique was used to study the pharmacological properties of fluoxetine.

[Establishment of heterologous expression model of hSERT in Xenopus laevis oocytes].

Aim: To determine the feasibility of establishing the heterologous expression model of human- serotonin transporter(hSERT or 5-HTT).

Methods: cRNA of SERT was transcribed from cDNA, which was cloned in the pOTV vector. Each oocyte of mature xenopus laevis was injected with transcribed cRNA in vivo and incubated at room temperature for 4-9 days.

[The sinus node itself also plays a role in heart rate slowing down during postnatal development].

The slowing down mechanism of heart rate during growth of the body after birth was studied in isolated rabbit heart and sinus node (SN) preparation with Langendorff perfusion method, conventional microelectrode recording and perforated patch for recording pacemaker current I(f). The radioimmunoassay was also used to measure the concentration of cAMP within SN cells. The results indicate that without the influence of nervous and humoral factors, the spontaneous heart rate would also become slower as the rabbit grew older, which is due to the decrease of spontaneous depolarized rate of phase 4 in SN cells.