• The Korean Journal of Physiology and Pharmacology
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• 제6권4호
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• pp.173-181
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• 2002

The sinoatrial (SA) node is a complex and inhomogeneous tissue in terms of cell morphology and electrical activity. There are two models of the cellular organisation of the sinoatrial node: the gradient and mosaic models. According to the gradient model there is a gradual transition in morphology and electrical properties of SA node cells from the centre to the periphery of the SA node. In the mosaic model, there is a variable mix of atrial and sinoatrial node cells from the centre to the periphery. This review focuses on the cellular organisation of the rabbit sinoatrial node in terms of the expression of connexin (Cx40, Cx43 and Cx45), L-type $Ca^{2+}$ channel and $Na^+-Ca^{2+}$ exchanger proteins. These immunocytochemical data, together with morphological and electrophysiological data, obtained from the intact sinoatrial node and isolated sinoatrial node cells support the gradient model of the cellular organisation of the SA node. The complex organisation of the sinoatrial node is important for the normal functioning of the sinoatrial node: (i) it allows the sinoatrial node to drive the surrounding hyperpolarized atrial muscle without being suppressed by it; (ii) it helps the pacemaker activity of the sinoatrial node continue under a wide range of physiological and pathophysiological conditions; (iii) it helps protect the sinoatrial node from reentrant arrhythmias.

• Journal of Chest Surgery
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• 제27권5호
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• pp.339-344
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• 1994

Sinus node dysfunction is common after orthotopic heart transplantation.Electrophysiologic studies have documented a high incidence [46% to 50%] of impaired sinus node automaticity and sinoatrial conduction in the early posttransplantation period. Sinus node dysfunction persists in over 20 % of patients and leads to prolonged bradyarrythmias, including sinus or nodal bradycardia and sinus arrest.The purpose of this paper was to observe sinus node dysfunction after orthotopic heart transplantation. Ten cardiac recipient dogs were monitored continuously after orthotopic transplantations between unrelated adult mongrel dogs. Crystalloid cardioplegic solution [Choongwoi Cardioplegia

• The Korean Journal of Physiology
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• 제19권2호
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• pp.127-137
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• 1985

The present study was undertaken in order to investigate effect of ethanol extract of Rehmanniae radix(RREE) on electrophysiology of sinus node and papillary muscle. Rehmanniae radix is a herbal medicine which has been known to have diuretic, antipyretic, hemopoietic and cardiotonic effects. Action potentials were recorded by means of glass capillary microelectrode(technique) in rabbit sinoatrial nodal cells and papillary muscle cells which were superperfused with either tyrode solution or tyrode solutions containing different amount of RREE. The results obtained were as follows ; 1) In both central and peripheral nodal cells maximum diastolic potential (MDP) and amplitude of action potential (APA) were not affected by RREE. 2) Action potential duration as expressed $APD_{60}$(time to 60% repolarization) of central and peripheral pacemaker cells were significantly prolonged following perfusion with tyrode solution containing 0.1% RREE. 3) The rates of spontaneous firing from central pecemaker cell were decreased by RREE at concentration of 0.05% and 0. 1% while spontaneous rhythm of perinodal cell was decreased by 0.1% RREE. 4) The action potential duration of papillary muscle as expressed $APD_{60}$ were prolonged by 0.1% RREE.

• The Korean Journal of Physiology
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• 제19권2호
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• pp.113-125
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• 1985

Electrophysiological difference of the central and peripheral area of the sinoatrial node in the rabbit was studied by glass microelectrode technique. Effects of $K^+,\;Na^+,\;Cs^+,$ adrenaline and ouabain on the action potential of the two areas were investigated, and transient hyperpolarization ($K^+-induced$ hyperpolarization) which developed following readmission of potassium after having pre-treated with $K^+-free$ Tyrode solution for 10 minutes was analyzed. The results obtained were as follows ; 1) The frequency of the spontaneous action potential recorded in the periphery of the SA node was faster than the central area. Reduction by $Cs^+$ and increase by O mM $K^+$, $10^{-6}M$ adrenaline and $10^{-6}M$ ouabain in the frequency of action potential were noticed more prominently in the peripheral than the central area. On the contrary, the frequency in the central area was more decreased than the Peripheral area by 13 mH $K^+$ and 1 mM $Co^{2+}$. 2) The amplitude of the K+_induced hyperpolarization was very small in the central area but large in the peripheral area. Transient hyperpolarization was abolished by ouabain and low sodium, and decreased by cooling the tissue $(17^{\circ}C)$. 3) By changing the concentration of $Ca^{2+}$ in the perfusate, the amplitude and the rate of transient hyperpolarization were increased in the high $Ca^{2+}$ concentration. It could be concluded that the central area of the SA node is less susceptible to the inhibition of Na-Pump and more susceptible to Ca-blocker and high concentration of $K^+$. The Na-Pump activity of the central area measured by means of transient hyperpolarization is found to be much less active than that of the peripheral area.

• The Korean Journal of Physiology
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• 제20권2호
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• pp.165-174
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• 1986

The voltage clamp studies were undertaken to elucidate the properties of the slow inward current, $i_{si}$, in the small preparations of the rabbit sinoatrial node. The slow inward current, $i_{si}$, which is known to be responsible for the late one-third of pacemaker potential and whole range of upstroke phase of action potential was analysed with the effects of isoprenaline, cobalt, ouabain and higenamine. The results obtained are as follows; 1) Voltage of SA node preparation was held at zero current level, usually-40mV and the slow inward current, $i_{si}$, was activated by depolarizing clamp pulses. Peak values of $i_{si}$, in steady state were at $-10{\pm}0mV$ in most preparations. 2) Isoprenaline, ${\beta}-agonist$ increased $i_{si}$ and no shift was noticed in voltage-dependency. 3) Cobalt ion in the concentration of 1 mM abolished is, in entire range of membrane potential and the difference of two current levels before and after $Co^{2+}$ treatment could be considered as pure $i_{si}$ magnitude. 4) In the therapeutic concentration of ouabain $(5{\times}10^{-8}M)$ slightly increased is, and reduced the time to reach the peak value. 5) Higenamine $(10^{-6}M)$ changed the configurations of action potential (i. e. rapid upstroke phase and notch in the spike) and increase spontaneous rate. It also increased is, and the effect of higenamine was blocked ${\beta}-blocker$, propranolol $(10^{-6}M)$.

• The Korean Journal of Physiology
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• 제19권2호
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• pp.101-111
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• 1985

Transient inward current (TI) was studied by the two micro-electrode voltage clamp technique in the sinoatrial node of the rabbit. The author confirmed that in $10^{-6}$ M ouabain TI was found in the SA node and investigated the effects of ions, $(Na^+,\;K^+,\;Ca^{2+})$, $\beta-agonist$ (isoprenaline), local anesthetics (quinidine, lidocaine) and Ca-blockers ($Co^{2+}$, verapamil, diltiazem) on the TI recorded during depolarizing voltage clamp pulses to -40 and -20 mV. The results obtained were as follows ; 1) $10^{-6}M$ ouabain increased the frequency of sinus action potential and decreased the amplitude, especially overshoot of action potential. TI was induced by the depolarizing voltage clamp Pulses and the magnitude of the slow inward current (isi) decreased and the time course was slowed by the same depolarizing pulses. 2) 30% $Na^{+}$ and 24mM $K^+$ decreased by $10^{-6}M$ ouabain and 6 mM $Ca^{2+}$ and $10^{-7}M$ isoprenaline increased TI, $i_{si}$ and current oscillations. 3) Quinidine $(5\times10^{-7}M)$ reduced TI and $i_{si}$ but lidocaine $(10^6\;-10^5M)$ didn't reduced or increase TI. Current oscillations increased and isi decreased by lidocaine. 4) Ca-blockers decreased the amplitude and the frequency of sinus action potential. TI and $i_{si}$ decreased significantly but were not abolished completely at the concentrations used in this experiment. Verapamil and diltiazem had inhibitory action on TI in $2\times10^{-7}M$ concentration and showed very slow recovery after wasting out with normal Tyrode solution.

• 한국임상수의학회지
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• 제25권5호
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• pp.391-395
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• 2008

8세령 수컷 요크셔테리어 잡종견(몸무게: 7.5kg)이 운동불내성과 실신을 주증상으로 강원대학교 동물병원에 내원하였다. 초기 심장 검사에서 경미한 이첨판 역류증이외에 특별한 이상소편은 관찰되지 않았다. 운동내성검사에서 환자는 심각한 chronotrophic incompetence소견을 보였고, 1시간-디지털 심전도 검사에서 돌발적으로 발생하여 종료되는 발작성 동성 빈맥소견(심박수: 156-172회)을 보였다. 추가적인 미주신경 자극시험과 verapamil 반응시험에서 빈맥이 종료되는 소견을 보였다. 이러한 소견을 토대로 본 증례는 동방회귀성 빈맥증으로 진단내렸다. 환자는 diltiarem과 enalapril로 치료하였고, 한달 후 재검사에서 운동 불내성 소견은 지속적으로 보였지만, 추가적인 실신소견은 관찰되지 않았다.

• The Korean Journal of Physiology
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• 제17권1호
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• pp.1-11
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• 1983

1) 토끼동방결절의 작은 절편에 미세 전극 두개로 voltage clamp를 하고 과분극에 의하여 활성화되는 내향전류, $i_f$의 동력학적 성상을 분석하였다. 2) 전류 $i_f$는 $10^{-7}g/ml$ TTX와 2 mM $Mn^{2+}$의 존재하에서 과분극 pulse에 의하여 활성화되었으며 그 범위는 $-45\;mV{\sim}-75\;mV$였다. 전류의 크기와 시간경과는 막전압이 과분극될수록 커지고 빨라졌다. 3) Envelope test결과 $i_f$전류는 단일 gate에 의하여 지수합수적 (exponential)으로 조절됨을 보였다. 4) 2 mM의 $Ba^{2+}$에 의하여$i_f$전류의 크기는 감소하고 시간경과도 느려졌으며 반응속도상수와 gating molecule의 열리고 닫히는 반응계수(rate coefficient; ${\alpha}_s$, ${\beta}_s$)와 막전압 관계곡선을 과분극쪽으로 이동시켰다. 이러한 $Ba^{2+}$의 효과는 24 mM $K^+$에 의하여 일부 상쇄되었다.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1996년도 정기총회 및 학술발표회
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• pp.5-5
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• 1996

In sino-atrial node cells which act as the normal pacemaker of the heart, K conductance in resting state is minimal due to the absence of inward rectifier K channels K conductance only increases when the membrane is depolarized by the activation of the delayed rectifier K current I$\_$k/. In the present study, we investigated the gating mechanism of$\_$k/ using the whole cell patch clamp technique in isolated single sinoatrial cells of the rabbit. (omitted)

• The Korean Journal of Physiology
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• 제18권1호
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• pp.19-35
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• 1984

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.