• The Korean Journal of Physiology
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• v.21 no.2
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• pp.179-189
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• 1987

Since it has been known that ryanodine has a potent negative inotropic effect on the cardiac muscle contractility (Jenden and Fairhurst, 1968), ryanodine has been a subject of intensive research (Frank and Sleator, 1975; Jones et al, 1978; Sutko et al, 1985). However, the underlying mechanism for the ryanodine dependent negative inotropic effect is still uncertain. In this study, the effects of ryanodine on the generation and relaxation of contracture due to Na-withdrawal and on the force-frequency relationship of heart muscles isolated from rats and guinea pigs were measured in an effort to understand the underlying mechanism of the ryanodine-induced negative inotropy. Results are summerized as follows: 1 ) Ryanodine significantly reduced the contractility of heart muscles produced at low frequency of stimulation, but showed a little effect on the contractility at high frequency stimulation. 2) Ryanodine, at the concentrations ranging from $10^{-6}\;M$ to $10^{-8}\;M$, had no significant effect on the Na-dependent relaxation of Na-withdrawl contracture. 3) Ryandoine significantly reduced the amplitude of the Na-withdrawl contracture, and this inhibitory effect was reinforced by procaine, antiagonized by caffeine and high potassium. From these results, it may be concluded that the negative inotropic effect of ryanodine is mainly due to an inhibition of calcium release from sarcoplasmic reticulum.

• The Korean Journal of Pharmacology
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• v.10 no.1 s.15
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• pp.21-39
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• 1974

Certain metabolic aspects of halothane's cardiac depressant action on the contractility of the myocardium were elucidated from a sudy of the effect of pyruvate on halothane-depressed rat atria. Approximately 6 mg% halothane was required to maintain a 50% depression of the contractility of rat atria suspended in a modified Krebs-Ringer bicarbonate glucose medium, pH 7.4, $30^{\circ}C$ for a 2 hr. period. Pyruvate was found to restore partially the contractility of halothane-depressed atria. The maximally effective concentration of pyruvate was 2.5 mM. There was minimal pyruvate effect on the force of contraction of control atria. The effect of pyruvate on halothane-depressed atria was shown to be due to the pyruvate and not the sodium ion of the sodium pyruvate. Pyruvate was found to produce no increase in the contractility of atria depressed by hypertonic medium, but caused a further depression. Selected aspects regarding the action of halothane on glucose metabolism in myocardial cells are discussed. The results are consistent with the hypothesis that at least a part of the negative inotropic action of halothane is due to an inhibition of glucose uptake or utilization in the glycolytic pathway.

• The Korean Journal of Malacology
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• v.25 no.1
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• pp.15-22
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• 2009

Because it is known that bivalve hearts contain various modulatory systems activated by neuroendocrine substances, it was examined whether different classes of endogenous and synthetic drugs of neuroendocrinological importance can influence cardiac functions of the Pacific oyster Crassostrea gigas. Cholinergically active agents acetylcholine and carbachol increased heart rates while diminishing cardiac contractility. Adrenergically active substances norepinephrine (NE) and epinephrine (Epi) also induced heart rate increase and contractility decrease. An $\alpha_1$-adrenergic receptor-selective agonist phenyephrine (PE) failed to modulate either parameter. The Epi-induced heart rate increase and contractile depression were both blocked significantly by non-selective $\beta_1/\beta_2$-adrenergic antagonist propranolol. A $\beta_1$-selective antagonist atenolol prevented Epi-induced heart rate decrease but not the contractile depression, suggesting possible $\beta_2$ receptors for Epi-induced contractile depression. The three autacoids examined exerted discrete responses: histamine increased heart rate and depressed contraction; $\gamma$-amino-butyric acid increased both parameters; serotonin failed to change either parameter. The 5 piscine anesthetic agents examined, MS-222, benzocaine, quinaldine, urethane, pantocaine and pentobarbital, all failed to influence the cardiac function of oysters. Collectively, activities of neuroendocrinologically acting agents in mammals showed unexpected and distinct activities from those in mammalian cardiovascular systems. These results obtained from substances of different physiological functions can serve as a basis for understanding neuroendocrine control of the heart function in Pacific oyster.

• Journal of Sensor Science and Technology
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• v.31 no.1
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• pp.6-11
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• 2022

To date, various techniques have been utilized to assess the contractility of cardiomyocytes and their response to drug-induced toxicity. However, these techniques are either invasive or involve complex fabrication methods and expertise. Here, we introduce the use of video-based analysis software to track the motion of cardiomyocytes and assess their contractility. The software, called "Tracker", is freely available and this is the first attempt at using it for cardiac contractility measurement. We used the software to measure the contractile properties of cells cultured on a rigid substrate and two flexible polydimethylsiloxane (PDMS) substrates having different elastic moduli day-wise up to eight days. Contractility was found to be highest in the most flexible substrate. Subsequently, the cardiotoxicity response of the cells on three different substrates was analyzed with verapamil. It was observed that the cells on rigid substrate were primarily affected by drug-induced toxicity, while the drug had a lesser impact on cells on the more flexible PDMS substrate. Evidently, the flexible substrate aided the maturation of cells and had lower drug toxicity, while the cells on PS could not fully mature. The assessment of cardiomyocytes using "Tracker" proved to be simple and reliable.

• Proceedings of the KIEE Conference
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• 1988.07a
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• pp.727-730
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• 1988

In this paper, cardiac parameters and relationship between stroke volume and impedance change were explained, and an impedance cardiograph was designed and constructed, and its accuracy was verified by experiment. Useful cardiac parameters such as stroke volume and contractility of cardiac muscle were measured noninvasively. The reproducibility of the instrument was measured to be better(less than 10%) than that of clinical standard method such as thermodilution. Hence impedance cardiography was found to be better technique for monitoring stroke volume and contractility of patients for pre and post operation, and pharmacological studies.

• Proceedings of the KSME Conference
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• 2007.05b
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• pp.2941-2946
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• 2007

A model of the cardiovascular system coupling cell, hemodynamics and autonomic nervecontrol function is proposed for analyzing heart mechanics. We developed a comprehensive cardiovascular model with multi-physics and multi-scale characteristics that simulates the physiological events from membrane excitation of a cardiac cell to contraction of the human heart and systemic blood circulation and ultimately to autonomic nerve control. Using this model, we delineatedthe cellular mechanism of heart contractility mediated by nerve control function. To verify the integrated method, we simulated a 10% hemorrhage, which involves cardiac cell mechanics, circulatory hemodynamics, and nerve control function. The computed and experimental results were compared. Using this methodology, the state of cardiac contractility, influenced by diverse properties such as the afterload and nerve control systems, is easily assessed in an integrated manner.

• Journal of Biomedical Engineering Research
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• v.9 no.1
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• pp.109-116
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• 1988

In this paper, principles of impedance tenchinque and relationship between stroke volume and impedance change were theoretically explained. An impedance cardiograph was designed and constructed. Its reproducibility was verified by experiment. Until now, the peak point of dZ/dt waveform, first derivative of impedance change(${\Delta}$Z) , has been detected by software technique requiring considerable time to process. However in this paper its peak point was found using hardware for saving processing time. Useful cardiac parameters such as stroke volume and contractility of cardiac muscle were measured noninvasively. The reproducibility of the instrument was measured to be better(less than 10%) than that of clinical standard method such as thermodilution (more than 30%). Hence impedance cardiography was found to be better techique for monitoring stroke volume and myocardial contractility for pre and post operation, and pharmacological studies.

• Proceedings of the Korean Biophysical Society Conference
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• 2001.06a
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• pp.17-17
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• 2001

It is well known that myocardial stretch causes changes in electrical signalling and contractility of the heart. For example, mechanical stretch depolarises the membrane potential of cardiac cells and alters the shape of action potentials. As a result, these effects either accelerate the frequency of heart rate or induce arrhythmias of the heart.(omitted)

• The Korean Journal of Physiology
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• v.30 no.2
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• pp.237-247
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• 1996

This study was carried out to determine the effect of $-6^{\circ}$ head-down bedrest on the cardiovascular and hormonal responses to orthostasis and to evaluate the mechanism of orthostatic intolerance. Ten healthy young men were changed the body position from $-6^{\circ}$ head-down or supine bedrest for 2 hr to $70^{\circ}$ head-up tilt for 20 min. During the bedrest, there were no differences in hemodynamic and hormonal changes between the head-down and the supine positions. However, the tendency of decreased end-diastolic volume and increased cardiac contractility during the later period of 2 hr showed that the cardiovascular adaptation could be accelerated within a relatively short period in the head-down bedrest. During the head-up tilt, presyncopal signs were developed in five subjects of the supine bedrest, and one of the same subjects of the head-down bedrest. In the tolerant subjects, the increase in cardiac contractility and plasma epinephrine level during the bend-up tilt was greater following the head-down bedrest than that following the supine bedrest to compensate for reduced venous return. The intolerant subjects showed the greater decrease in end-diastolic and stroke volume, and the greater increase in heart rate during the head-up tilt than the tolerant subjects. Cardiac contractility and plasma epinephrine level were remarkably increased. However, arterial pressure was not maintained at the level for the appropriate compensation of the reduced venous return. It seems that the tolerance to orthostasis is more effective after the short-term head-down bedrest than after the supine bedrest, and the secretion of epinephrine induces the higher cardiac performance as a compensatory mechanism fur the reduced venous return during the orthostasis following the head-down bedrest than the supine bedrest.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.615-621
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• 1999

In spite many evidences has supported the cardioprotective effect of bradykinin, its direct effects at the cell level are still under question. We investigated the both effects of bradykinin (BK) on $Ca^{2+}-related$ ionic currents using whole cell voltage clamp technique in rabbit cardiomyocytes and on the intracellular $Ca^{2+}$ transient using calcium sensitive fluorescence dye, indo-1AM. Simultaneously with recording intracellular $Ca^{2+}$ transients, cell contractility was estimated from the changes in length of the electrical stimulated rat cardiac myocytes. L-type $Ca^{2+}$ current decreased by bradykinin at the entire voltage range. Inward tail current increased initially up to its maximum about 4 min after exposing myocytes to BK, and then gradually decreased again by further exposure to BK. This tail current decreased remarkably at washing BK off but slowly recovered ca. 20 min later. The change in cell contractility was similar to that in tail current showing initial increase followed by gradual decrease. Removal of BK brought remarkable decrease in contractility, which was recovered $15{\sim}20$ min after cessation of electrical stimulation. Bradykinin increased $Ca^{2+}$ transient initially but after some time $Ca^{2+}$ transient also decreased coincidentally with contractility. From these results, it is suggested that bradykinin exerts directly its cardioprotective effect on the single myocytes by decreasing the intracellular $Ca^{2+}$ level followed by an initial increase in $Ca^{2+}$ transient.