• Proceedings of the Korean Society of Precision Engineering Conference
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• 2012.10a
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• pp.891-892
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• 2012

• The Korean Journal of Physiology
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• v.27 no.1
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• pp.67-77
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• 1993

Acute and chronic effects of ethanol (EOH) administration on the cardiovascular and hormonal responses to repeated hemorrhage were investigated in conscious normotensive Wistar rats and spontaneously hypertensive rats (SHR). The chronic EOH treated group received 5% EOH (vol/vol) ad libitum in the drinking water far the first week,10% for the last 2 weeks, and 20% for the last 5 weeks from the age of 6 weeks. The EOH free group received tap water. Chronic EOH and EOH free groups were randomly subdivided into acute EOH infusion and control groups. Under ether anesthesia, catheters were inserted into the femoral vein and both femoral arteries. After rats regained consciousness and their blood pressure was stabilized, responses to quick hemorrhage (5 ml/kg BW) were tested. In the acute EOH infusion group, hemorrhage was induced 20 min after EOH infusion (1.0 g/kg BW), Baroreceptor reflex sensitivity was assessed by the ratio of changes in hen.1 rate and mean arterial pressure (${\Delta}HR/{\Delta}MAP$) immediately after the hemorrhage. Chronic EOH administration elevated MAP in Wistar rats. During acute EOH infusion, MAP do- creased and HR increased in all groups. In comparison to EOH free control rats, acute or chronic EOH treated rats showed a greater reduction in MAP and a smaller elevation in heart rate in response to a hemorrhage. The degree of MAP reduction was significantly greater in SHR than in Wistar rats. Both the acute and chronic EOH administration attenuated the baroreceptor reflex and retarded MAP recovery, again the trend being much more prominent in SHR. The increase in plasma vasopressin and lenin concentrations after hemorrhage were intensified by the chronic EOH administration. SHR showed a greater vasopressin response but a smaller lenin response than Wistar rats. These results indicate that the EOH treated rats, particularly SHB, are prone to shock by a hemorrhage, which may be partly attributed to an impaired baroreceptor reflex function.

• 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.29 no.1
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• pp.91-102
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• 1995

The role of neurohumoral mechanisms in the regulation of cardiovascular functions and the effects of ethanol (EOH) on these mechanisms were examined in hemorrhaged conscious Wistar rats. The rats were bled at a constant rate (2 ml/kg/min) through the femoral artery until mean arterial pressure (MAP) was reduced by 30 mmHg. We studied the responses to hemorrhage 1) under normal conditions (Normal), and after pretreatments with 2) neural blockade (NB), pentolinium, 3) arginine vasopressin V1-receptor antagonist (AVPX) + NB, 4) angiotensin II ATI-receptor antagonist (AngIIX) + NB, 5) combined humoral blockade (HB), and 6) neurohumoral blockade. Intravenous administration of 30% EOH (6.3 ml/kg) attenuated the baroreceptor reflex sensitivity, and enhanced the depressor action of AngIIX. During hemorrhage, NB produced a faster fall ill MAP than Normal both in the saline and EOH groups. However, HB accelerated the rate of fall in MAP only in the EOH group. The recovery from hemorrhagic hypotension was not different between NB and Normal rats, but was attenuated in HB rats in the saline group. Under NB, AngIIX, but not AVPX, retarded the recovery rate compared with NB alone. EOH attenuated the recovery of MAP after hemorrhage in Normal rats, but completely abolished the recovery in HB rats. We conclude that 1) the maintenance of MAP during hemorrhage is mediated almost entirely by the autonomic functions, 2) angiotensin II plays an important role in the recovery from hemorrhagic hypotension, but AVP assumes little importance, 3) AVP release largely depends on the changes in blood volume, whereas renin release depends on the changes in blood pressure rather than blood volume, and 4) EOH increases the dependence of cardiovascular regulation on angiotensin II and impairs the recovery from hemorrhagic hypotension through the attenuation of autonomic functions.

• 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.

• 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.

• 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.

• Korean Journal of Anesthesiology
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• v.71 no.6
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• pp.453-458
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• 2018

Background: Pain on injection is a limitation with propofol use. The effect of the Valsalva maneuver on pain during propofol injection has not been studied. This maneuver reduces pain through the sinoaortic baroreceptor reflex arc and by distraction. We aimed to assess the efficacy of the Valsalva maneuver in reducing pain during propofol injection. Methods: Eighty American Society of Anesthesiologists class I adult patients undergoing general anesthesia were enrolled and divided into two groups of 40 each. Group I (Valsalva) patients blew into a sphygmomanometer tube raising the mercury column up to 30 mmHg for 20 seconds, while Group II (Control) patients did not. Anesthesia was induced with 1% propofol immediately afterwards. Pain was assessed on a 10-point visual analog scale (VAS), where 0 represented no pain, and 10, the worst imaginable pain, and a 4-point withdrawal response score, where 0 represented no pain, and 3, the worst imaginable pain. Scores were presented as median (interquartile range). Results: We analyzed the data of 70 patients. The incidence of pain was significantly lower in the Valsalva than in the control group (53% vs. 78%, P = 0.029). The withdrawal response score was significantly lower in the Valsalva group (1.00 [0.00-1.00] vs. 2.00 [2.00-3.00], P < 0.001). The VAS score was significantly lower in the Valsalva group (1.00 [0.00-4.00] vs. 7.00 [6.25-8.00], P < 0.001). Conclusions: A prior Valsalva maneuver is effective in attenuating injection pain due to propofol; it is advantageous in being a non-pharmacological, safe, easy, and time-effective technique.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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• pp.89-94
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• 2004

The arterial pressure is regulated by the nervous and humoral mechanisms. The neuronal regulation is mostly carried out by the autonomic nervous system through the rostral ventrolateral medulla (RVLM), a key area for the cardiovascular regulation, and the humoral regulation is mediated by a number of substances, including the angiotensin (Ang) II and vasopressin. Recent studies suggest that central interleukin-1 (IL-1) activates the sympathetic nervous system and produces hypertension. The present study was undertaken to elucidate whether IL-1 and Ang II interact in the regulation of cardiovascular responses to the stress of hemorrhage. Thus, Sprague-Dawley rats were anesthetized and both femoral arteries were cannulated for direct measurement of arterial pressure and heart rate (HR) and for inducing hemorrhage. A guide cannula was placed into the lateral ventricle for injection of IL-1 $(0.1,\;1,\;10,\;20\;ng/2\;{\mu}l)$ or Ang II $(600\;ng/10\;{\mu}l)$. A glass microelectrode was inserted into the RVLM to record the single unit spike potential. Barosensitive neurons were identified by an increased number of single unit spikes in RVLM following intravenous injection of nitroprusside. I.c.v. $IL-1\;{\beta}$ increased mean arterial pressure (MAP) in a dose-dependent fashion, but HR in a dose-independent pattern. The baroreceptor reflex sensitivity was not affected by i.c.v. $IL-1\;{\beta}$. Both i.c.v. $IL-1\;{\alpha}\;and\;{\beta}$ produced similar increase in MAP and HR. When hemorrhage was induced after i.c.v. injection of $IL-1\;{\beta}$, the magnitude of MAP fall was not different from the control. The $IL-1\;{\beta}$ group showed a smaller decrease in HR and a lower spike potential count in RVLM than the control. MAP fall in response to hemorrhage after i.c.v. injection of Ang II was not different from the control. When both IL-1 and Ang II were simultaneously injected i.c.v., however, MAP fall was significantly smaller than the control, and HR was increased rather than decreased. These data suggest that IL-1, a defense immune mediator, manifests a hypertensive action in the central nervous system and attenuates the hypotensive response to hemorrhage by interaction with Ang II.