• Journal of Chest Surgery
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• v.47 no.4
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• pp.398-401
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• 2014

Severe tricuspid regurgitation resulting from a flail leaflet is a rare cause of neonatal cyanosis. We report a neonate with profound cyanosis and severe tricuspid regurgitation caused by a rupture of the papillary muscle supporting the anterior leaflet, without other structural heart defects. Ductal patency could not be established. The repair of the tricuspid valve was performed after initial stabilization by using extracorporeal membrane oxygenation.

• The Korean Journal of Physiology
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• v.17 no.1
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• pp.45-54
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• 1983

Contractile responses of myocardium and vascular smooth muscle to angiotensin II were studied in isolated rabbit papillary muscles and aortic helical strips, with respect to the sensitivity and the mechanism of action. All experiments were performed in $HCO-_3\;-buffered Tyrode solution which was aerated with $3%\;CO_2-97%\;O_2$ and kept pH 7.35 at $35^{\circ}C$. Action potentials were measured by conventional microelectrode technique in the papillary muscles. Helical strips of vascular smooth muscle were prepared from the descending thoracic aorta of the rabbit. Angiotensin II elicited a positive inotropic effect in doses from $10^{-8}$ to $10^{-6}\;M$, and this effect was dose-dependent and characterized by a symmetrical increase of maximum dP/dt during contraction and relaxation phase. Slow responses (or slow action potentials) were induced by A. II $(10^{-6}\;M)$ in the papillary muscle hypopolarized by 27 mM $K^+$. These A. II-induced slow action potentials were eliminated by verapamil (2 mg/l), but not affected by propranolol $(10^{-5}\;M)$. In aortic helical strips, contractile force was increased dose-dependently in the range of $10^{-10}{\sim}10^{-7}\;M$ A. II. $ED_{50}$ in aorta was $3{\times}10^{-9}\;M$ A. II, whereas that in paillary muscle was $2.5{\times}10^{-7}\;M$ A. II. A. II contracted vascular smooth muscle in depolarizing concentration of $K^+$ (100 mM $K^+$), and also produced a sustained contraction even in the presence of verapamil and regitine. The results of this experiment suggest that the primarily important physiological role of A. II is the action on the blood vessel, and the positive inotropic effect of A. II in papillary muscle results from the increase of slow inward $Ca^{++}$ current, and that A. II-induced contraction of aorta is independent of transmembrane potential and associated with promoting bet transmembrane $Ca^{++}\;-influx$ and the mobilization of cellular $Ca^{++}$.

• The Korean Journal of Physiology
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• v.29 no.2
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• pp.203-216
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• 1995

The effects of ${\alpha}_1-adrenergic$ receptor stimulation on membrane potential, intracellular $Na^+$ activity, and twitch force were investigated in ventricular muscles from guinea-pig hearts. Action potentials, intracellular $Na^+$ activity, and twitch force of ventricular papillary muscles were measured simultaneously under various experimental conditions. Stimulation of the ${\alpha}_1-adrenergic$ receptor by phenylephrine produced variable changes in action potential duration, a slight hyperpolarization of the diastolic membrane potential, a decrease in intracellular $Na^+$ activity, and a biphasic inotropic response in which a transient negative inotropic response was followed by a sustained positive inotropic response. These changes were blocked by prazosin, an antagonist of the ${\alpha}_1-adrenergic$ receptor, but not by atenolol, an antagonist of the ${\beta}-adrenergic$ receptor. This indicates that the changes in membrane potential, intracellular $Na^+$ activity, and twitch force are mediated by stimulation of the ${\alpha}_1-adrenergic$ receptor, but not by stimulation of ${\beta}-adrenergic$ receptor. The decrease in intracellular $Na^+$ activity was not observed in quiescent muscles, depending on the rate of the action pontentials in beating muscles. The intracellular $Na^+$ activity decrease was substantially inhibited by tetrodotoxin. However, the decrease in intracellular $Na^+$ activity was not affected by an inhibition of the $Na^+-K^+$ pump. Therefore, the decrease in intracellular $Na^+$ activity mediated by the ${\alpha}_1-adrenergic$ receptor appears to be due to a reduction of $Na^+$ influx during the action potential, perhaps through tetrodotoxin sensitive $Na^+$ channels. Our study also revealed that the decrease in intracellular $Na^+$ activity might be related to the transient negative inotropic response. The intracellular $Na^+$ activity decrease could lower intracellular $Ca^{2+}$ through the $Na^+-Ca^{2+}$ exchanger and thereby produce a decline in twitch force.

• Journal of Chest Surgery
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• v.43 no.4
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• pp.413-416
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• 2010

A 47-year-old man presented with complaints of chest pain and dyspnea caused by deceleration injury due to an automobile accident. Systolic cardiac murmur was audible at the right sternal border. An electrocardiogram showed sinus tachycardia. Transthoracic echocardiography revealed a flailing anterior leaflet of the tricuspid valve, papillary muscle rupture, and severe valve insufficiency. Rupture of papillary muscle of the anterior leaflet and chordae tendineae of the posterior leaflet were confirmed by right atrial incision under routine cardiopulmonary bypass. Artificial chordae tendineaes were implanted between the anterior and posterior leaflet and papillary muscles in the right ventricles. De-Vega annuloplasty was also added. This is a very rare case in which a surgery was done for tricuspid valve regurgitation caused by post-traumatic papillary muscle rupture.

• The Korean Journal of Physiology
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• v.16 no.1
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• pp.13-23
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• 1982

Effects of external pH and potassium concentrations on the electrical and mechanical properties were investigated on rabbit papillary muscle. Papillary muscles were perfused in horizontal chamber with Tris Tyrode solutions and action potential along with isometric tension was recorded simultaneously. Potassium concentrations were varied between 1 and 12 mM at low(6.9), normal(7.4) and high (7.9) external pH. The following results were obtained: 1) On rasing the potassium concentration from 1 to 12 mM resting membrane potentials decreased from $-88.8{\pm}2.8$ to $-66.4{\pm}1.2\;mV$ at normal pH and the amplitude of action potential decreased from $115.1{\pm}0.7$ to $97.5{\pm}2.8\;mV$. On lowering the potassium concentration, membrane hyperpolarized and at 1 mM potassium concentration resting potentials were $-107{\pm}2.2\;mV$. Duration of action potential especially $APD_{60}{\sim}APD_{90}$ increased($APD_{90}$: $214{\pm}15.8\;ms$ at 1 mM $K^+$ to $287{\pm}18.1\;ms$ at 12 mM $K^+$). 2) During acidosis membranes hyperpolarized by more than 20 mV within 1 min. and then slow recovery was observed during the following 10 min. During alkalosis membranes depolarized about 10 mV, which were maintained until washing with normal Tyrode solutions. 3) On lowering the external pH(7.9-6.5), duration of action potential increased progressively and it was most prominent at pH 6.5 and $K^+$ 1mM. 4) Magnitude of developed tension was $0.6{\pm}0.14\;g/mm^2$ at normal pH and potassium concentration (stimulus frequency : 60/min). Relative isometric tension to normal value increased along the increment of stimulus frequency($44.2{\pm}4.2%$ at 6/min to $271{\pm}86.7%$ at 180/min). Force-frequency relations were altered quantitatively during the perfusion with different external pH solutions. 5) Developed tension did not show marked variation within the range of $2{\sim}8\;mM$ potassium concentrations. Positive inotropism was observed at less than 2 mM $K^+$ and negative inotropism beyond 12 mM $K^+$ concentrations. From the above results we concluded that the effects of potassium ion concentration on electrical and mechanical properties of rabbit papillary muscle are related to the changes in surface negative charge due to acid base disturbances.

• Toxicological Research
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• v.16 no.3
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• pp.211-219
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• 2000

The therapeutic effect of AS2-006A, a derivative of asiaticoside, has been studied and is being developed as a new wound-healing agent. In the present study, the general pharmacological effects on 1) central nervous system, 2) autonomic nervous system, 3) respiratory system, 4) gastrointestinal system. 5) cardiovascular system. and 6) urinary system were assessed in experimental animals and in in vitro models. 1. In vivo animal study: External applications of the 1 % gel ointment of AS2-006A to rats at the doses of 200. 600 or 2000 mg/kg body weight showed no observable pharmacological effects. The effects on the central nervous system were assessed by observation of behavior, hexobarbital-induced sleeping time, pentetrazole-induced convulsion assay, body temperature measurements, and observations on spontaneous activity and catalepsy. The gel ointment exhibited no effects on the cardiovascular system (i.e. blood pressure and heart rate), renal physiology (i.e. urine volume and electrolytes excretion) and gas-trointestinal physiology (i.e. intestinal charcoal propulsion and gastric mucosal irritation). 2. In vitro experiments: The effects of AS2-006A on the physiology of smooth and cardiac muscles were assessed. Muscle contractions were isotonically and isometrically measured in organ chambers using a physiograph. Cumulative additions of AS2-006A (10$^{-9}$ -10$^{-5}$ M) induced no changes in the tension of isolated guinea pig ileum and tracheal muscles. AS2-006A only slightly increased contractility of rat atrial and papillary muscles at 10$^{-2}$ M, which was not statistically different from control. These data showed that the gel ointment of AS2-006A could be externally applied as a wound-healing agent with no potential side effects.

• Journal of Chest Surgery
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• v.14 no.1
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• pp.33-39
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• 1981

In the presence of severe non-calcific mitral regurgitation, a dilated mitral annulus, absence of severe subvalvular chordal thickening, and no major loss of leaflet substance, reconstructive surgery for mitral regurgitation is a reasonable approach. Between March, 1980 to November, 1980, 5 patients underwent mitral annuloplasty using Carpentier Ring for severe mitral regurgitation. All 5 cases were of rheumatic in origin. There were no ruptured chorda tendinae or ruptured papillary muscles except slight thickening of the leaflet. There was no operative or late death. As is Carpentier`s report, in patient with severe mitral regurgitation who meet above criteria, mitral annuloplasty using Carpentier Ring is preferable to valve replacement.

• Korean Journal of Veterinary Research
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• v.43 no.1
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• pp.31-39
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• 2003

We have investigated the effect of extracellular $Mg^{2+}$ ($[Mg^2+]_o$) on action potential duration (APD) in guinea pig papillary muscles by using microelectrodes. Increasing $[Mg^2+]_o$ resulted in progressive negative inotropic effect, progressive ascending depolarization of membrane potential, and increase in intracellular $Mg^{2+}$ concentration. In addition, increase in $[Mg^2+]_o$ from 1.1 to 3, 6, 10, and 20 mM produced a reversible dose-dependent shortening of both APD at 30% ($APD_{30}$) and 90% repolarization ($APD_{90}$), especially showing a tendency towards more remarkable prominent shortening in $APD_{30}$ than $APD_{90}$. Cooling from 37 to 33 and $27^{\circ}C$ diminished the $[Mg^2+]_o$-induced APD shortening. Increase in extracellular $Ca^{2+}$ concentration from 1.8 to 3.6 and 5.4 mM caused a significant depressed effect on the increasing $[Mg^2+]_o$-induced APD shortening. Furthermore, increase in $[Mg^2+]_o$ from 1.1 to 10 and 20 mM produced a significant depressed effect on the APD shortening induced by extracellular $Ca^{2+}$. Pretreatment of verapamil and imipramine significantly attenuated the increasing $[Mg^2+]_o$-induced APD shortening in both $APD_{30}$ and $APD_{90}$, whereas the $[Mg^2+]_o$-induced APD shortening was not affected by strophanthidin, glibenclamide and tetrabutylammonium. These findings suggest that the effects of $[Mg^2+]_o$ on APD are probably due to a decrease in ionic transport across plasma membrane. In conclusion, the present study indicates that $[Mg^2+]_o$ exerts antiarrhythmic activities by antagonistic actions on intracellular $Ca^{2+}$.

• Korean Journal of Head & Neck Oncology
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• v.14 no.1
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• pp.88-93
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• 1998

In order to review the clinicopathologic characteristics of the thyroid cancer associated with benign thyroid disease, we evaluated 47 patients treated between January, 1993 and September, 1997 at the Chonnam National University Hospital. In those period, we had operated a total of 690 thyroidectomy of which 320 were diagnosed as thyroid cancer. Forty three(91.4%)occurred in women and four(8.5%)occurred in men. The mean age at operation was 46.7years(range, 15 to 76 years). Forty three of the 47 cancers(91.4%) were papillary carcinomas while 4(8.5%)were follicular. Twenty four of the 47 patients (51%) were occult thyroid carcinomas measured less than 1 cm in diameter. The concurrent benign disease were nodular goiter(n=17), Hashimoto's thyroiditis(n=16), follicular adenoma(n=10), Graves' disease(n=2) and diffuse hyperplasia(n=2). Thirty one patients were diagnosed by preoperative FNAC and they underwent total thyroidectomy. Three were diagnosed by frozen section examination at the time of operation. Among them, one underwent total thyroidectomy and two underwent subtotal thyroidectomy. Eight cases revealed lymph node metastases and 2 cases extended to surrounding muscles. In conclusion, concurrent thyroid cancers and benign thyroid disease are not uncommon and a regular ultrasonic follow-up with selective aspiration cytologic examination is recommaned to enhance their diagnostic accuracy.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.229-236
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• 1995

The effect of ${\alpha}_1$-adrenoceptor(${\alpha}_1$-AR) stimulation on intracellular pH($pH_i$), $Na^+$ activity($a_{Na}{^i}$) and contractility were investigated in isolated papillary muscles of euthyroid or hyperthyroid guinea pig with conventional microelectrode, $Na^+$ or $H^+$-selective microelectrodes, and tension transducer. Stimulation of the ${\alpha}_1$-AR by phenylephrine produced a decrease in $a_{Na}{^i}$ in euthyroid preparations. This decrease in $a_{Na}{^i}$ was abolished in presence of PKC activator, phorbol dibutyrate, and increased contrary to decrease. Phenylephrine also increased $a_{Na}{^i}$ in hyperthyroid ones. However, phenylrephtine produced an increase in $pH_i$ in both euthyroid and hyperthyroid ones. These changes were blocked by prazosin, an antagonist of ${\alpha}_1$-AR. These findings suggest that the changes in $a_{Na}{^i}$ and $pH_i$ are mediated by a stimulation of $Na^+-H^+$ exchange via ${\alpha}_1$-AR stimulation. This study focused on the increase in $a_{Na}{^i}$, $pH_i$ and contractility. The increase in $pH_i$ was blocked by amiloride or EIPA, $Na^+-H^+$ exchange inhibitors. Therefore, the increase in $a_{Na}{^i}$ and $pH_i$ mediated by ${\alpha}_1$-AR appeared to be due to an influx of $Na^+$ and a reduction of $H^+$ through $Na^+-H^+$ exchange. This study also revealed that the increase in $pH_i$ and $a_{Na}{^i}$ might be related to the sustained positive inotropic response. The $a_{Na}{^i}$ increase may contribute to the intracellular $Ca^{2+}$ through the $Na^+-Ca^{2+}$ exchange, and the $pH_i$ increase could cause an increase in the $Ca^{2+}$ sensitivity of myofilaments and may augment the ${\alpha}_1$-AR-mediated positive inotropic response.