• Journal of Biomedical Engineering Research
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• v.24 no.4
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• pp.329-337
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• 2003

Blood in congenital or acquired AY fistula(arteriovenous fistula) flows from arteries directly to veins. detouring peripheral micro-circulation. This makes a great effect on the hemodynamics of human cardiovascular system. In this study, a computational method using lumped parameter mode) was proposed to simulate the cardiovascular hemodynamics of patients with acute AV fistula The cardiovascular system model with a fistula compartment in left lower limb was built using 17 standard lumped compartments. Using fourth order Runge-Kutta method. we solved numerically the unsteady linear set of the ordinary differential equations resulting from application of Kirchhoff's law to the lumped parameter hemodynamic model. The baroreceptor reflex system was implemented to explain the auto-regulation effect of the cardiovascular system with acute AV fistula.

• Journal of Biomedical Engineering Research
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• v.22 no.5
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• pp.393-402
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• 2001

A computational model representative of cardiovascular circulation was built using 12 standard lumped compartments. Especially, both the baroreceptor reflex and the cardiopulmonary reflex control model were implemented to explain the auto-regulation of cardiovascular system. Another important aspect of this model is to utilize the impulse-response curve of the nerve system in transferring the impulse error signals to autonomous nerve system. For the verification of this model, we have computed the normal hemodynamic conditions and compared those with the clinical data. Then. hemodynamic shock of 20% hemorrhage to cardiovascular system was simulated to test the effects of the control system model. The results of these two simulations were well matched with the experimental ones. The steady state LBNP simulation was also performed. The transient changes of hemodynamic variables due to ramp increase of bias pressure of LBNP showed good agreement with the physiological experiments. Numerical solution using only the baroreflex model showed relatively a larger deviation from the experimental data. compared with the one using the control model haying both the baroreflex and the cardiopulmonary reflex systems, which shows an important role of the cardiopulmonary reflex system for the simulation of the hemodynamic behavior of the cardiovascular system .

• The Korean Journal of Physiology
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• v.9 no.2
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• pp.23-31
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• 1975

The effects of ethanol intravenously administered on the mean arterial blood pressure and heart rate responses to electrical stimulation of vagus nerve and the hypothalamus were studied in the cats. Also investigated were the effects of ethanol on the cardiovascular responses to bilateral carotid occlusion and to intravenously injected epinephrine and acetylcholine separately. The results obtained from the present study were as follows; 1. In 1.0 ml/kg and 2.0 ml/kg of ethanol infused groups the mean arterial blood pressure increased gradually and reached plateaus in 10 minutes after ethanol infusion while no marked changes in blood pressure were observed in 0.5 ml/kg of ethanol infused group. 2. The pressor responses elicited by the electrical stimulation of the hypothalamus were depressed directly proportionally to amount of ethanol infused. In 0.5 ml/kg of ethanol infused group the pressor response was reduced to 84.5% of control value and it declined to 17.0% of control in 2.0 ml/kg of ethanol infused group. 3. After ethanol administration the heart rate decreased slightly and also was decreased positive chronotropic effect elicited by hypothalamic stimulation. In several cases even negative chronotropic responses were observed during electrical stimulation in the hypothalamus. 4. Since the pressor responses to bilateral carotid occlusion was reduced by ethanol administration it is suggested that activity of baroreceptor is inhibited by ethanol. 5. No changes were observed in the negative chronotropic effect Produced by electrical stimulation of the vegus nerve of ethanol infused animal. And cardiovascular responses to intravenously injected epinephrine and acetylcholine were not influenced by ethanol either.

• The Korean Journal of Physiology
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• v.5 no.2
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• pp.71-78
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• 1971

Anesthetized dogs were tilted from horizontal to the upright and head down position. Tilting to the upright position was followed by an increase in heart rate. In the head down position a decreased heart rate was obtained. The arterial blood pressure was decreased in the upright position and was decreased markedly in the head down position. The central venous pressure was decreased in the upright position and was markedly decreased down to the negative pressure in the head down position. The respiratory rate was slightly increased in the upright position comparing to that in the horizontal position. No remarkable changes were noted in the head down position. From the above results the following factors were discussed The decreased arterial blood pressure during the upright position was supposed to be the secondary effect from the diminished venous return that was suggested by the decreased central venous pressure. The decreased arterial blood pressure in the head down position was also supposed as the above reason as the diminished central venous pressure during the tilt. In addition the cardioinhibitory effects originated from the baroreceptors might have been operated during head down tilting. In the heart rate there was slight tachycardia in the upright position this was assumed as the abolished cardioinhibitory impulses from the baroreceptor in the upright position. On the contrary, despite of the decrease of arterial blood pressure in the head down position as well as in the upright, the bradycardia have been appeared. This was suggestive of cardioinhibitory impulses from the baroreceptors which was stretched during head down tilting. From the above findings there is a possibility of continous cardioinhibitory responses during head down tilting for this kind of the short period of 10 minutes which was chosed in this study.

• Proceedings of the KOSOMBE Conference
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• v.1997 no.05
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• pp.165-170
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• 1997

In this paper, we consider the aortic sinus baroreceptor, which is the most representative baroreceptors sensing the variance of pressure in the cardiovascular system(CVS), and propose heart activity control model to observe the effect of delay time in heart period and stroke volume under the regulation of baroreflex in arotic sinus. The proposed heart activity baroreflex regulation model contains CVS electric circuit sub-model, baroreflex regulation sub-model and time delay sub-model. In these models, applied electric circuit sub-model is researched by B.C.Choi and the baroreflex regulation sub-model transforms the input, the arotic pressure of CVS electric circuit sub-model, to outputs, heart period and stroke volume by mathematical nonlinear feedback. We constituted the time delay sub-model to observe sensitivity of heart activity baroreflex regulation model by using the variable value to represent the control signal transmission time from the output of baroreflex regulation model to efferent nerve through central nervous system. The simulation object of this model is to observe variability of the CVS by variable value in time delay sub-model. As simulation results, we observe three patterns of CVS variability by the time delay. First, if the time delay is over 2.5 sec, arotic pressure, stroke volume and heart rate is observed nonperiodically and irregularly. Second, if the time delay is from between 0.1 sec and 0.25 sec, the regular oscillation is observed. Finally, if time delay is under 0.1 sec, then heart rate and arotic pressure-heart rate trajectory is maintained in stable state.

• The Korean Journal of Pain
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• v.19 no.2
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• pp.202-206
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• 2006

Background: Stellate ganglion block (SGB) might be associated with changes in the blood pressure (BP) and heart rate (HR). The heart rate variability (HRV) shows the balance state between sympathetic and parasympathetic activities of the heart. The changes in these parameters of the HRV were studied to evaluate the possible mechanism of SGB in changing the BP. Methods: SGB was performed on 26 patients, using a paratracheal technique at the C6 level, and 8 ml of 1% mepivacaine injected. The success was confirmed by check the Horner's syndrome. The BP, HR and HRV were measured before and 5, 15, 30, 45 and 60 minutes after the SGB. Results: The increases in the BP from the baseline throughout the study period were statistically, but not clinically significant. The HR and LF/HF (low frequency/high frequency) ratio were increased at 5 and 45 min, respectively, after the administration of the SGB. In a comparison of left and right SGB, no significant differences were found in the BP, HR and HRV. A correlation analysis showed that an increased BP was significantly related with the changes in the LF/HF ratio and LF at 15 and 30 minutes, respectively, after the SGB. Dividing the patients into two groups; an increased BP greater and less than 20% of that at the baseline INC and NOT groups, respectively, hoarseness occurred more often in the INC group (P = 0.02). Conclusions: It was concluded that SGB itself does not clinically increase the BP and HR in normal hemodynamic patients. However, the loss of balance between the sympathetic and parasympathetic nerve system, attenuation of the baroreceptor reflex and hoarseness are minor causes of the increase in the BP following SGB; therefore, further studies will be required.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.275-281
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• 2015

Orthostatic hypotension is most common in elderly people, and its prevalence increases with age. Attenuation of the vestibulo-sympathetic reflex (VSR) is commonly associated with orthostatic hypotension. In this study, we investigated the role of glutamate on the vestibulo-solitary projection of the VSR pathway to clarify the pathophysiology of orthostatic hypotension. Blood pressure and expression of both pERK and c-Fos protein were evaluated in the nucleus tractus solitarius (NTS) after microinjection of glutamate into the medial vestibular nucleus (MVN) in conscious rats with sodium nitroprusside (SNP)-induced hypotension that received baroreceptor unloading via sinoaortic denervation (SAD). SNP-induced hypotension increased the expression of both pERK and c-Fos protein in the NTS, which was abolished by pretreatment with glutamate receptor antagonists (MK801 or CNQX) in the MVN. Microinjection of glutamate receptor agonists (NMDA or AMPA) into the MVN increased the expression of both pERK and c-Fos protein in the NTS without causing changes in blood pressure. These results indicate that both NMDA and AMPA receptors play a significant role in the vestibulo-solitary projection of the VSR pathway for maintaining blood pressure, and that glutamatergic transmission in this projection might play a key role in the pathophysiology of orthostatic hypotension.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.4
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• pp.353-358
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• 2014

Control of blood pressure is maintained by the interaction between the arterial baroreflex and vestibulosympathetic reflex during postural changes. In this study, the contributions of vestibular receptors and baroreceptors to the maintenance of blood pressure following acute hypotension were compared in terms of phosphorylated extracellular regulated protein kinase (pERK) expression in the nucleus tractus solitaries (NTS). Expression of pERK in the NTS was measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or sinoaortic denervation (SAD) 5, 10, 20, and 40 min following acute hypotension induced by sodium nitroprusside (SNP) infusion. Expression of pERK increased significantly in the NTS in the control group following SNP infusion, and the expression peaked at 10 min after SNP infusion. The number of pERK positive neurons increased following SNP infusion in BL, SAD, and BL+SAD groups, although the increase was smaller than in control group. The BL group showed a relatively higher reduction in pERK expression than the SAD group, and the pERK expression in the NTS was localized to the caudal portion of the nuclei in the BL and SAD groups. These results suggest that the vestibular receptors may play a key role in maintaining blood pressure following acute hypotension; thus, the vestibular system may contribute to compensate for orthostatic hypotension.

• The Korean Journal of Physiology
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• v.10 no.1
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• pp.55-59
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• 1976

Most investigators have come to stress two different concepts of mechanism controlling renin release; intrarenal baroreceptor theory and the macula densa theory(Vander 1967, Thurau and Masson 1974). In the macula densa theory, the specific macula densa parameter, most commonly suggested as a possible signal, is either the osmolality or the concentration of sodium in the tubular fluid (Thurau 1964, Vander and Miller 1964, Reeves and Sommers 1965). It has been shown that sodium plays an important role in the release of renin either in vivo (Thurau 1964, Vander and Miller 1964, Thurau et al 1972) or in vitro experiments(Oelkers et al 1970, Hammerson et al 1971, Michelakis 1971). On the other hand the osmolality appears to have no effect on the release of renin in vivo (Vander 1967, Thurau and Masson 1974). However, there has been little attempt to study the effect of osmolality on in vitro renin release. We therefore undertook the present investigation to elucidate the effect of osmolality on renin release and to further test the sodium influence upon the release of renin from isolated kidney slice preparations. Isolated renal cortical slices were washed with normal Krebs-Hensenleit bicarbonate buffer solution and incubated for 30 minutes in a medium containing an appropriate concentration of sodium and osmolality. The renin released into the medium was measured by the method of radioimmunoassay(Haber et al 1969). The results obtained are as follows; 1. The release of renin from renal cortical slices was progressively inhibited as the sodium concentration in the medium increased. 2. No significant alteration in renin release was observed when osmolality of the medium was changed. These results suggest that the release of renin from the renal cortical slices is directly affected by the changes in sodium concentration in the medium, but is not influenced by the alterations in osmolality.

• Sleep Medicine and Psychophysiology
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• v.6 no.1
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• pp.19-25
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• 1999

Sleep alters both breathing pattern and the ventilatory responses to external stimuli. These changes during sleep permit the development or aggravation of sleep-related hypoxemia in patients with respiratory disease and contribute to the pathogenesis of apneas in patients with the sleep apnea syndrome. Fundamental effects of sleep on the ventilatory control system are 1) removal of wakefulness input to the upper airway leading to the increase in upper airway resistance, 2) loss of wakefulness drive to the respiratory pump, 3) compromise of protective respiratory reflexes, and 4) additional sleep-induced compromise of ventilatory control initiated by reduced functional residual capacity on supine position assumed in sleep, decreased $CO_2$ production during sleep, and increased cerebral blood flow in especially rapid eye movement(REM) sleep. These effects resulted in periodic breathing during unsteady non-rapid eye movement(NREM) sleep even in normal subjects, regular but low ventilation during steady NREM sleep, and irregular breathing during REM sleep. Sleep-induced breathing instabilities are divided due primarily to transient increase in upper airway resistance and those that involve overshoots and undershoots in neural feedback mechanisms regulating the timing and/or amplitude of respiratory output. Following ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include 1) hypocapnia, 2) inhibitory effect from lung stretch, 3) baroreceptor stimulation, 4) upper airway mechanoreceptor reflexes, 5) central depression by hypoxia, and 6) central system inertia. While the respiratory control system functions well during wakefulness, the control of breathing is commonly disrupted during sleep. These changes in respiratory control resulting in breathing instability during sleep are related with the pathophysiologic mechanisms of obstructive and/or central apnea, and have the therapeutic implications for nocturnal hypoventilation in patients with chronic obstructive pulmonary disease or alveolar hypoventilation syndrome.