PubMed Health⌕ Search

Biomedical subjects

T F Liu

Publications and source records attributed to T F Liu.

At least 37 records · Page 2Linked to original sources
PubMed1995

Comparison of early afterdepolarization induced by cesium chloride in mouse atrial and ventricular fibers.

AIM: To study the similarities and the differences in the induction of early afterdepolarization (EAD) by CsCl, a blocker of potassium channels, between mouse atrial and ventricular fibers. METHODS: Papillary muscle from left ventricle or a small piece of right atrium of Swiss Albino mouse was isolated. Transmembrane action potential (AP) and EAD were recorded using the conventional microelectrode method. RESULTS: CsCl induced EAD directly in the mouse atrial and ventricular fibers on the basis of elongation of action potential duration (APD). In both preparations EAD appeared after 5-15 min exposure to CsCl and the take-off potentials (TOP) were in the same range (-30 to -60 mV). But the inducing concentration in ventricular fibers (3 mmol.L-1) was lower than that in atrial fibers (5 mmol.L-1), and most of the EAD induced in atrium belonged to the triggered burst type (6/9) which demonstrated the property of cycle length (CL)-dependence while the EAD occurred in ventricle mainly belonged to the second plateau type (14/17) which showed no definite relation with the CL. CONCLUSION: Low concentration of CsCl induced EAD more easily in mouse ventricular fibers than in atrial fibers, and the types of EAD were also different from each other. These suggested that there might be some differences in potassium channels between mouse atrial and ventricular fibers.

Action Potentials↗
PubMed1995

[Characterization of outward current in mouse ventricular myocytes].

Depolarization-activated, calcium-independent outward currents (Iout) in enzymatically dispersed mouse ventricular myocytes were characterized by whole-cell recording technique. During brief depolarizations to potentials positive to -50 mV, outward K+ currents in these cells rise rapidly to a peak followed by a slower decay to an apparent plateau. The relative peak to plateau amplitudes in a single cell varied as a function of the holding potential (HP) from which the currents were evoked. Reversal potentials for the peak and plateau components were -64.3 +/- 3.9 mV and -53.3 +/- 2.9 mV, respectively (uncorrected for junction potentials). The outward current decay is well described by double exponential fits, whereas the time course of peak Iout decay following a 500 ms prepulse is best fitted by single exponential function, indicating the presence of two distinct components, IKf and IKs, of the outward currents in mouse ventricular cells. Application of 4-AP were accompanied by a marked attenuation of peak Iout and plateau Iout, indicating that both IKf and IKs display similar sensitivities to 4-AP. The steady state inactivation of IKf is found incomplete within the test potential range (-80 - +30 mV) owing probably to the fact that the APD of mouse myocardium is too short.

Animals↗
PubMed1994

Characteristics of early afterdepolarization in mouse atrial fibers.

Early afterdepolarization (EAD) in mouse atrial fibers was investigated under the treatment with aconitine, 3.0 mmol/L K+, quinidine, ryanodine or Bay k 8644. All of these EADs possessed the following common characteristics: all the parameters of EAD showed cycle length-dependence; take-off potential of the first triggered burst played an important role in the generation of the other parameters; hyperpolarization of the triggered brust enhanced the end of EAD; and the second plateau response might be used as an indicator of the capability of EAD generation of myocardiac cell. All those EADs were inhibited or abolished by nifedipine, tetrodotoxin or lidocaine. Potassium channel activators, lemakalim, thalium ion, acetyl-choline or high potassium could also inhibit or abolish the EADs. It is suggested that the EADs induced by different agents may base on a common mechanism: all currents contributing to the plateau phase of the action potential play an important role in the generation of EAD.

Aconitine↗
PubMed1993

A reevaluation of the critical membrane potential of the effective refractory period in guinea pig ventricular fibres.

The traditional critical membrane potential (CMP), -55(-)-60 mV, which corresponds to effective refractory period (ERP), was anew investigated in guinea pig ventricular muscle fibres. The electrical and contractile responses to the stimulus during repolarization of action potential (AP), particularly from +10 to -60 mV, were observed. One third of 35 tested cells displayed testing action potential (TAP) and local response at > or = -54 mV when they were stimulated by testing pulses in 37 degrees C normal Tyrode's solution. Potential level of TAP which occurred earliest was at -30 mV and that of local response which appeared earliest was at 0 mV during repolarization among 95 systematic tests. Most of the TAPs belonged to the slow response potential type. The ratio of TAP evoked at > or = -54 mV initial membrane potential (IMP) was as high as 86% when the experiment was carried out in 37 degrees C 1.5 mmol KC1/L Tyrode's solution. In view of distribution of IMPs of TAPs, the CMP of ERP in guinea pig ventricular muscle fibres was more positive than traditional CMP measured by Hoffman et al. in dog, sheep Purkinje fibres and had a quite changeable range. The CMP of every cell in ventricular muscle was not all the same, and their CMPs approximated to normal distribution. There was no sharp line separating ERP from relative refractory period in myocardium. Higher temperature and low [K]0 were the important factors elevating CMP of ERP.

Action Potentials↗
PubMed1993

Effects of pinacidil and acetylcholine on early afterdepolarization of atrial fibers in mouse heart.

The effects of pinacidil and acetylcholine (Ach) on action potential (AP) and early afterdepolarization (EAD) were investigated in mouse atrial fibers. Under treatment with pinacidil the AP and EAD were affected only with the concentration of 8 x 10(-5) M, which inhibited EAD but did not affect AP except for only a minor reduction of action potential duration (APD). After withdrawal of pinacidil, the inhibitory effect of EAD was enhanced. Under treatment with Ach (2 x 10(-7) M), AP was not changed except the APD, which was significantly reduced, and the EAD was completely abolished. Withdrawal of Ach produced a rebound increase in APD and led to induction of EAD or promoted EAD to more extensive level such as appearance of long second plateau. Atropine (1 x 10(-7) M) abolished the rebound effect caused by withdrawal of Ach. The mechanism of EAD generation induced by removing Ach is discussed.

Acetylcholine↗
PubMed1992

Effects of lemakalim and thalium on early afterdepolarization in mouse atrial fibers.

The effects of lemakalim (BRL 38227) and thallium ion (Tl) on action potential (AP) and on early afterdepolarization (EAD) were studied in mouse atrial fibers. Under treatment with lemakalim (25 mcM) or Tl (0.2 mM), the AP was not significantly changed except for the reduction of duration of AP (APD). EAD induced by 3.0 mM K superfusion was abolished by 50 mcM lemakalim and only partially inhibited or was not effected under 25 mcM lemakalim. However, EAD was abolished completely and rapidly by Tl treatment. With addition of K concentration in superfusate to 5.0 mM the EAD could only be partially inhibited. By further increasing the K concentration to 7.0 mM the EAD could be completely abolished. It is suggested that the activator of outward current could inhibit EAD as well as the blockers of inward currents.

Action Potentials↗
PubMed1992

Effects and mechanism of low [K]o on the critical potential of effective refractory period in guinea pig ventricular muscle cells.

1.5 mM KCl Tyrode's solution enabled the critical potential (-55-60 mV) of effective refractory period to shift in a positive direction in guinea pig ventricular muscle cells. In 1.5 mM KCl Tyrode's solution, the probability of testing AP's initial potential positive to -54 mV in the repolarizing phase was as high as 80% (n = 10), but the percentage in 4.5 mM [K]o group was only 11% (n = 35). The mean value of the positive shift was 30.2 +/- SD 17 mV. Testing APs had higher values of overshoots (mean = 23 +/- 13.8 mV); their mean Vmax was 98 V/s. Early after depolarization and positive inotropic effects appeared. 13.5 mM KCl, in contrast to 1.5 mM KCl, produced contrary effects. Phenomena indicated that early after depolarization in low [K]o was associated with the positive shift of critical potential of effective refractory period. Above-mentioned effects of 1.5 mM KCl could not be completely eliminated by verapamil, but could be abolished by an inactivation promoting agent of sodium channel, lidocaine 7.4 x 10(-5) M (n = 10). The results suggest that accelerating recovery time and shifting recovery potential in the positive direction of inactivated sodium channel might be the principal reasons for the effects of low [K]o. The role of the Na+ pump inhibitor, ouabain, was not similar to that of 1.5 mM KCl Tyrode's solution except for positive inotropic effect.

Animals↗
PubMed1991

Role of take-off potential and second plateau response in generation of early afterdepolarization in arterial fibers of mouse heart.

Take-off potentials (TOPs) of triggered bursts were studied on aconitine- 3.0 mM K+ and quinidine-induced early afterdepolarization (EADs) in mice atrial fibers. TOPs varied from -40 to -66 mV (-53.4 +/- 6.4 mV, n = 14) depending on the cycle length of stimulation. TOPs were cycle length-dependent and the relationship between TOP and cycle length was exponential. Before the generation of EAD, a second plateau appeared following the rapid repolarization phase of action potential (AP). In some preparations, EAD could not be induced, especially at a shorter cycle length, leaving a definite second plateau following the AP under treatment with effective agents. By application of a premature stimulation on the second plateau, only one burst could be observed. However, two or more bursts could be induced when a stimulation was applied on the rapid repolarization phase at -50 +/- 6 mV (n = 17) level. We defined this phenomenon as "second plateau response" which was studied in the present work under treatment with quinidine (4 cases), 3.0 mM K+ (4), ryanodine (6) and Bay K 8644 (3). The second plateau response was abolished by tetrodotoxin (1.0 microM), nifedipine (2.0 microM) or rapid driving. All of these were similar to the properties of the EAD. It is suggested that the second plateau response may be taken as an indicator of the capability of the EAD generation in myocardiac cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Role of afterhyperpolarization in termination of early afterdepolarization in mouse atrial fibers.

Afterhyperpolarization (AHP) following triggered burst in early afterdepolarization (EAD) was investigated in mouse atrial fiber treated with aconitine or ryanodine. In both cases, a long second plateau (SP) with or without intermittent trains of bursts could be observed in certain conditions. Repolarization potentials were measured both in normal EAD (cycle lengths of 1-5 sec) and in EAD with a long SP. The values of repolarization potentials were almost constant, around -61 mV, in both situations. AHP could be recorded at the end of the intermittent bursts or after a burst elicited by an electrical stimulation on the long lasting SP. When the voltage of AHP attained the repolarization potential, rapid repolarization started instantly leading to complete repolarization of the EAD. It is suggested that AHP in EAD or following a burst elicited by stimulation enhances the termination of EAD.

Aconitine↗
PubMed1991

[Effects of nicardipine on automaticity of sinoatrial node in rabbit heart].

The dual effects of nicardipine (Nic) on the automatic activity of sinoatrial (SA) node cell in rabbit heart had been observed using intracellular microelectrodes. Superfused with Nic 0.1, 0.5, 1.0, and 5.0 mumol.L-1 for 10 min, the spontaneous rate was decreased by 32%, 42%, 47%, and 69%, respectively. However, by superfusing with Nic 0.05 mumol.L-1, the spontaneous rate and the amplitude of action potentials were increased by 12% and 13% respectively. Nic 5.0 mumol.L-1 inhibited the positive chronotropic effects of isoproterenol and nicotine. The results suggest that Nic may block the calcium influx in SA node cells.

Action Potentials↗
PubMed1991

Recent developments in diagnosis and treatment of nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is one of the major cancers that Chinese radiotherapists have to treat, because of its high incidence which shows a tendency to increase. Although results of radiotherapy in NPC have improved markedly during the last decade, treatment at an early stage of the disease is the most effective. It is therefore important to make the diagnosis early, and recently serological surveys by IgA/VCA show its efficacy in high risk populations. Histological diagnosis so far has not correlated to prognosis, and new histological classifications have been proposed by many authors. The importance of CT scans in diagnosis and treatment is stressed. Criteria for clinical staging of NPC will have to be reconsidered, especially the T staging, as 80% of cases formerly classified as T1 may already have paranasopharyngeal extension, as shown on CT scans. The technique of radiotherapy has not changed much essentially since the advent of telecobaltherapy. However, various institutions have their own special variations. The most striking advance is the use of high-dose rate afterloading brachytherapy as boost for residual disease or as main treatment for nasopharyngeal recurrences. Finally, the role of chemotherapy in the radiation treatment of NPC is discussed, and the paper concludes with some remarks on the future outlook in the diagnosis and treatment of NPC.

Humans↗
PubMed1990

Early afterdepolarization induced by ryanodine in atrial fibers of mouse heart.

The effects of ryanodine on the action potential and induction of early afterdepolarization (EAD) were studied in the atrial fibers of mouse heart. Under treatment with ryanodine, the duration of the action potential (ADP) was prolonged. The percentage of the prolongation of ADP25, APD50 and ADP100 were 83, 49 and 20%, respectively, at a cycle length of 1 sec driving stimulation. As the cycle length was prolonged (from 0.5-10 sec), EAD could be induced in 10 of 16 preparations showing exponential relationship with the cycle length. Tetrodotoxin, lidocaine and nifedipine inhibited the induction of EAD. In 6 preparations in which the EAD was not induced, more than one burst could respond to a single premature stimulation applied in the early phase of repolarization, which was defined as second plateau response. The mechanism of ryanodine-induced EAD has been investigated.

Action Potentials↗
PubMed1990

[Effects of nicotine on action potentials of guinea pig and rabbit papillary muscles].

The electrophysiological action of nicotine was studied by microelectrode technique on isolated guinea pig and rabbit papillary muscles. Nicotine had no significant effect on RP, APA and Vmax; but its biphasic effect on APD35, APD90 and ERP were observed in different concentrations, ie: high concentration (604 mumols/L) prolonged APD35, APD90 and ERP by 27.3, 26.0 and 26.1% respectively, whereas low concentration (0.6 mumol/L) shortened them by 49.6, 40.0 and 27.6%, respectively. It is suggested that high concentration of nicotine may enhance the calcium influx, but low concentration decrease it.

Action Potentials↗
PubMed1990

Early afterdepolarization in mouse atrial fibers induced by 3.0 mM K+ and the inhibitory effects of tetrodotoxin and nifedipine.

Early afterdepolarization (EAD) was induced under superfusion of Tyrode solution (K+ = 3.0 mM) at a longer cycle length in mouse atrial fibers. The relationships between the duration and the number of triggered bursts and cycle length were exponential (n = 17). Thus, EAD possesses the property of cycle length dependence. Under a moderate concentration of TTX (4.0 microM) or nifedipine (5.0 microM) treatment, EAD was partially inhibited but maintained cycle length dependence. When a high concentration of the drugs (30 microM and 8.0 microM, respectively) was applied, EAD was abolished at all cycle lengths of driving stimulation. It is suggested that both inward currents (INa and ICa) are involved in the generation of EAD in mouse atrial fibers.

Action Potentials↗
PubMed1990

[Effects of sodium vanadate on action potentials of guinea pig papillary muscles].

Sodium vanadate (NaVO3, 800 mumol/L) diminished the plateau phase and the action potential duration of the action potentials in guinea pig ventricular fibers (VF). 200 mumol/L also reduced the maximal rate of depolarization of slow action potentials in the partial depolarized VF under high K superfusion and inhibited the delayed after depolarization induced by adrenalin. It is suggested that NaVO3 may inhibit the slow channel current and does not reduce the sodium pump activity in VF significantly when it was used extracellularly.

Action Potentials↗
PubMed1989

10-year survival rate for patient with nasopharyngeal carcinoma after radiation therapy. Clinical analysis of 367 cases.

Of 1,344 patients with nasopharyngeal carcinoma treated during 1961-1965 at the Shanghai Cancer Hospital, 367 who survived over 10 years after radiation therapy, were analysed. The results showed that the patients with stage I, II nasopharyngeal carcinoma and those with stage III, IV, the 10-year survival rates were 41.5% and 22.8% respectively, the overall 10-year survival rate being 27.3%. The 10-year survival rate was higher for female patients than for males, and was not related to the age of the patients and the pathological type of this carcinoma. The optimal tumor dosage was thought to be 60-70 Gy 350(95.4%) out of the 367 patients received radiotherapy only once. The rest received repeated irradiation for recurrence. For the reirradiated patients, the 10-year survival rate was 13.5%. Most recurrences occurred 5 years after radiotherapy (12/17), and only 5 within 3 years.

Adolescent↗
PubMed1989

[Effects of nicotine on automaticity of sinoatrial node in rabbit heart].

The electro-physiological effects of nicotine on sinoatrial node cells in rabbit heart were studied using intracellular microelectrodes. When superfused with nicotine 604.0, 60.4, 6.0 or 0.6 mumol/L the spontaneous rate stopped or decreased for 20 s and then increased, eventually surpassing the control values 50 +/- 13, 45 +/- 12, 23 +/- 10 and 14 +/- 6%, respectively. The inhibitory phase was blocked by atropine and the excitatory phase was eliminated by tubocurarine chloride, hexamethonium bromide or pindolol. These results suggest that the effects observed may be related to cholinergic system and caused by nicotine induced catecholamine release.

Action Potentials↗