• 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.

• Journal of Chest Surgery
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• v.31 no.5
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• pp.441-450
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• 1998

The medullospinal tract cells are known to play an important role in the control of the cardiovascular activities. To clarify the modes of action of the neurotransmitters on these cells, glutamate, GABA(${\gamma}$-aminobutyric acid) and bicuculline were applicated iontophoretically into the rostral ventrolateral medulla in adult cats anesthetised with ${\alpha}$-chloralose. Followings are the results obtained : 1. The spontaneous activities of the cardiac-related neurons in rostral ventrolateral medulla (RVLM) were increased by the glutamate and decreased by the GABA. 2. Bicuculline, an antagonist of GABA, alone didn't increase the frequency of the action potentials, but could reverse the cellular response to the GABA, simultaneously applicated. 3. GABA seemed to decrease the peak as well as the basal discharge of the neurons in RVLM, but hardly changed their periodicities. 4. The cellular responses of RVLM evoked by the peripheral nerve stimulation could be inhibited by the iontophoretically released GABA. In conclusion, GABA seemed to act as an inhibitory neurotransmitter on the cardiac- related neurons in RVLM of the cats anesthetized with ${\alpha}$-chloralose. But the maintenance of the periodicities of these cells after the application of bicuculline suggested that the afferent activity of the baroreceptor didn't play a key role in the spontaneous activities of the RVLM neurons.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.1-11
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• 1989

In this study, it was aimed to investigate the role of serotonergic neurotransmission in nucleus tractus solitarius (NTS) for the central regulation of blood pressure and heart rate and its involvement in baroreceptor reflex activation in rats. A microinjection of 5-hydroxytryptamine (5-HT) into the NTS produced decreases in blood pressure and heart rate. Maximal decreases were $34.4{\pm}1.6$ mmHg and $41.7{\pm}10.2$ beats per min by 300 pmol of 5-HT. Microinjections of ${\alpha}-methylnor-adrenaline$ $({\alpha}-MNE)$ and clonidine manifested similar decreases in blood pressure and heart rate. The hypotensive and bradycardial effects of 5-HT were blocked by previous applications of 5-HT antagonists, ritanserin, methysergide and ketanserin into the NTS, respectively. By pretreatment with reserpine and 6-hydroxydopamine (6-OHDA, i.c.v.), both hypotensive and bradycardial effects of 5-HT were significantly attenuated. Pretreatment with 5, 7-dihydroxytryptamine (5,7-DHT, i.c.v.) enhanced the hypotensive and bradycardial effects of 5-HT. Similarly, following pretreatment with 6-OHDA, the effects of clonidine were increased. Pretreatment either with 5,7-DHT or 6-OHDA significantly attenuated the sensitivity of baroreflex produced either by phenylephrine or by sodium nitroprusside. When either 5,7-DHT or 6-OHDA was injected into the NTS $(5,7-DHT;\;8{\mu}g\;6-OHDA;\;10{\mu}g)$, both of the baroreflex sensitivities were impaired. In the immunohistochemical study, the injection of 6-OHDA into the the NTS led to reduction of axon terminal varicosity, however, the injection did not reduce the numbers of catecholaminergic cell bodies. Likewise, when 5,7-DHT was injected into the NTS, the varicosity of serotonergic axon terminals was markedly reduced. Based on these results, it is suggested that (1) stimulation of serotonergic receptors in the NTS leads to decreases in blood pressure and heart rate as observed with the stimulation of catecholaminergic system, (2) both serotonergic and catecholaminergic receptors may be located postsynaptically, and (3) the serotonergic neurons as well as catecholaminergic neurons may have a close relevance for the activation of baroreflex.

• The Korean Journal of Physiology
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• v.19 no.2
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• pp.139-153
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• 1985

The passive tilt has been performed to study the orthostasis on the cardiovascular system. The orthostasis due to upright tilt was demonstrated as follows: the venous return, cardiac output and systemic arteiral blood pressure were decreased, whereas there was concomitant increase of heart rate, through the negative feedback mediated by such as the baroreceptor . Previous investigators have suggested that the tolerance to the orthostasis could he increased by blocking the cholinergic fiber with atropine which prevented vasodilation and bradycardia through the vasovagal reflex during the orthostasis. However, this hypothesis has not been clearly understood. This study was attempted to clarify the effect of atropine on the tolerance of the cardiovascular system to the upright and head-down tilt, and to investigate the change of the blood flow through head and lower leg with Electromagnetic flowmeter in both tilts before and after atropine state. Fourteen anesthetized dogs of $10{\sim}14kg$ were examined by tilting from supine position to $+77^{\circ}$ upright position (orthostasis), and then to $-90^{\circ}$ head-down position (antiorthostasis) for 10 minutes on each test. And the same course was taken 20 minutes after intravenous administration of 0.5mg atropine. The measurements were made of the blood flow(ml/min.) on the carotid artery, external jugular vein, femoral artery and femoral vein. At the same time pH, $PCO_2$, $PO_2$ and hematocrit (Hct) of the arterial and venous blood, and heart rate(HR) and respiratory rate (RR) were measured. The measurements obtained from upright and head-down tilt were compared with those from supine position. The results obtained are as follows: In upright tilt, the blood flow both on the artery and the vein through head and lower leg were decreased, however the decrement of blood flow through the head was greater than the lower leg And the atropine attenuated the decrement of the blood flow on the carotid artery, but not on the vessels of the lower leg. HR was moderately increased in upright tilt, but slightly in head-down tilt. The percent change of HR after the atropine administration was smaller than that before the atropine state in both upright and head-down tilts. Before the atropine state, RR was decreased in upright tilt, whereas increased in head-down tilt. However after the atropine state, the percent change of RR was smaller than that of before the atropine state in both upright and head-down tilts. In upright tilt, venous $PCO_2$ was increased, but arterial $PO_2$ and venous $PO_2$ were slightly decreased. Hct was increased in both upright and head-down tilts. The findings of blood $PCO_2$, $PO_2$ and Hct were not interferred by the atropine. In conclusion, 1;he administration of atropine is somewhat effective on improving the cardiovascular tolerance to postural changes. Thus, atropine attenuates the severe diminution of the blood flow to the head during orthostasis, and also reduces the changes of HR and RR in both orthostasis and antiorthostasis.

• The Korean Journal of Physiology
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• v.21 no.2
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• pp.211-223
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• 1987

Head-down tilt (HDT) at $-6^{\circ}$ has been commonly used as the experimental model in both man and animals to induce the blood shift toward the head or central protion of the body, demonstrating similar physiological effect encountered in the weightlessness in the orbital flight. There are few reports about the physiological response upon the cardiovascular regulatory system or the tolerance to the $(-6^{\circ})$ HDT within a relatively short period less than 1 hour. Therefore, the purpose of this study way to observe the effects of $-6^{\circ}$ HDT on cardiovascular system within 30 minutes and to evaluate early regulatory mechanism for simulated hypogravity. Ten mongrel dogs weighing 8-12 kg were anesthetized with the infusion of 1% ${\alpha}-chloralose$ (100 mg/kg) intravenously, and the postural changes were performed from the supine to the $-6^{\circ}$ head-down Position, then from the head-down to the supine (SUP), and each posture was maintained for 30 minutes. Blood flow $({\dot{Q}})$ through common carotid and femoral arteries were determined by the electromagnetic flowmeter. Mean arterial pressure (MAP), heart rate (HR), respiratory rate , and pH, $P_{O_2}$, $P_{CO_2}$ and hematocrit (Hct) of arterial and venous blood were also measured. The peripheral vascular resistance was calculated by dividing respective MAP values by ${\dot{Q}}$ through both sides of common carotid or femoral arteries. The concentration of plasma epinephrine and norepinephrine was determined by Peuler & Johnson's radioenzymatic method. The results are summarized as follows: In the initial 5 minutes in $-6^{\circ}$ HDT, HR was significantly (p<0.05) increased and MAP slightly decreased. Although ${\dot{Q}}$ and carotid peripheral artery resistance were not significantly changed, ${\dot{Q}}$ through femoral artery was diminished and femoral peripheral artery resistance was elevated. In the SUP, the initial changes of MAP and HR were increased (p<0.05), but those of ${\dot{Q}}$ and peripheral vascular resistance through both common carotid and femoral arteries were not significant. After 10 minutes of each postural change in both HDT and SUP, MAP was maintained almost equal to that of the level of pretilting control. During 60 minutes of both postural changes of HDT and SUP, $P_{O_2}$ and Hct were not changed significantly. However pH tended to increase slowly and $P_{CO_2}$ was gradually decreased. The pH and $P_{CO_2}$ seemed to be related to the increased respiratory rate. Plasma epinephrine concentration was not changed significantly and plasma norepinephrine concentration was slightly decreased in the course of HDT and also at 10 minutes of SUP. However these concentration changes were statistically insignificant. From these results, it may be concluded that the effect of $-6^{\circ}$ HDT for 30 minutes on the cardiovascular system and plasma catecholamine levels of the dog is minimum and it is suggestive that the cardiovascular regulatory mechanism, possibly mediated by so called gravity receptors including baroreceptor and volume receptor, has been properly and adequately operated.