• 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.

• Journal of Pharmacopuncture
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• v.22 no.2
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• pp.95-101
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• 2019

Objectives: Angiotensin II (AngII), a major product of renin-angiotensin system (RAS) has important role in induction of hypertension and antihypertensive effect of several medicinal plant was mediated by effect on this agent. Therefore, this study examined the possible effect of hydroalcoholic extract of Crocus sativus (C. sativus) on hypertension induced by AngII. Methods: Six groups (n = 6) of rats were used as follow: 1) Control, 2) AngII (300 ng/kg), 3) Losartan (Los, 10 mg/kg) + AngII and 4-6) C. sativus extract (10, 20 & 40 mg/kg,) + AngII. The femoral artery and vein were cannulated for recording cardiovascular parameters and drugs administration, respectively. All drugs were injected intravenously (i.v). Los and all doses of C. sativus injected 10 min before AngII. Systolic blood pressure (SBP), mean arterial blood pressure (MAP) and heart rate (HR) were recorded throughout the experiment and those peak changes (${\Delta}$) were calculated and compared to control and AngII. Results: AngII significantly increased ${\Delta}MAP$, ${\Delta}SBP$ and ${\Delta}HR$ than control (P < 0. 01 to P < 0.001) and these increments were significantly attenuated by Los. All doses of C. sativus significantly reduced peak ${\Delta}MAP$, ${\Delta}SBP$, and ${\Delta}HR$ than AngII group (P < 0. 05 to P < 0.001). In addition, peak ${\Delta}MAP$, ${\Delta}SBP$ in doses 10 and 20 were significant than Los + AngII group (P<0.05 to P< 0.01) but in dose 40 only MAP was significant (P<0.05). Peak ${\Delta}HR$ in all doses of C sativus was not significant than Los+ AngII. Conclusion: Regarding the improving effect of the C. sativus extract on AngII induced hypertension, it seems that this ameliorating effect partly mediated through inhibition of RAS.

• Journal of Veterinary Clinics
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• v.21 no.2
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• pp.168-171
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• 2004

The effects of alterations of dose of xylaznie (X) and Zoltil$\circledR$ (TZ) on canine anesthesia were examined. Experimental groups were divided into three (Group 1: X 1.1 mg/kg and TZ 10 mg/kg, Group 2: X 1.65 mg/kg and TZ 7.5 mg/kg, Group 3: X 2.2 mg/kg and TZ 5 mg/kg), and each had 5 dogs. A femoral artery was catheterized for measurement of blood pressure, and baseline value was measured. The dogs were sedated with xylazine intramuscularly, then after 10 minutes TZ were injected intravenously. Mean arterial blood pressures (MAP), duration of analgesia, mean arousal time (MAT) and mean walking time (MWT) after TZ injection were measured, and the depth of analgesia and the quality of recovery were scored. The values of MAP were recorded from the time of pre-xylazine injection to arousal. Duration of analgesia and was assessed by tail clamping test, and which were done at 10 minutes intervals after TZ injection. The decreases of MAP from 40 minutes after TZ injection were significant (p<0.05). In group 2, MAP at 20 minutes, and from 40 minutes to arousal were significantly decreased (p<0.05). In group 3, MAP were significantly decreased from 40 minutes. MAT were 62.2$\pm$9.2 minutes in group 1, 60.2$\pm$7.5 minutes in group 2, and 71.0$\pm$6.9 minutes in group 3. MAT in group 3 was significantly increased compared with group 2 (p<0.05), and the differences of MWT among each groups were not significant (p>0.05). The scores of quality of recovery were significantly lowered in group 3 compared with group 1 or group 2, which means the side effects of recovery were less occurred. Thus, it was considered that the combination X 2.2 mg/kg IM and TZ 5 mg/kg IV is more effective to surgical procedures and to prevent long and rough recovery of Zoletil anesthesia.

• Journal of Dental Anesthesia and Pain Medicine
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• v.18 no.3
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• pp.169-175
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• 2018

Background: The objective of this study was to compare hemodynamic and recovery characteristics of total intravenous anesthesia using propofol target-controlled infusion (TCI) versus sevoflurane for extraction of four third molar teeth. Methods: One hundred patients undergoing extraction of four third molar teeth under general anesthesia were randomized to one of two groups. Group 1 received propofol TCI-oxygen for induction and propofol TCI-oxygen-air for maintenance. Group II received a propofol bolus of 2 mg/kg for induction and sevoflurane-oxygen-air for maintenance. Heart rate, mean arterial pressure (MAP), operating time, time to emergence, nausea and vomiting, and sedation and pain scores were measured in each group. Results: Demographic data, including age, gender, weight, and height, were not significantly different between the two groups. The MAP was significantly higher after intubation (P = 0.007) and injection of anesthesia (P = 0.004) in the propofol group than in the sevoflurane group, with significant reflex bradycardia (P = 0.028). The mean time to emergence from anesthesia using propofol was 25 s shorter than that of sevoflurane (P = 0.02). Postoperatively, the propofol group was less sedated than the sevoflurane group at 30 min (0.02 versus 0.12), but this difference was not significant (P = 0.065). Conclusion: Both propofol TCI and sevoflurane are good alternatives for induction and maintenance of anesthesia for short day-case surgery. However, propofol TCI does not blunt the hemodynamic response to sudden, severe stimuli as strongly as sevoflurane, and this limitation may be a cause for concern in patients with cardiac comorbidities.

• Journal of Chest Surgery
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• v.29 no.1
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• pp.1-6
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• 1996

We developed an experimental model of brain death using dogs. Brain death was induced by increasing the intracranial pressure (ICP) gradually by continuous Infusion of saline through an epidural Foley catheter in 5 mongrel dogs (weight, 18~22kg). Hemodynamic and electrocardiographic changes were evaluated continuously during the process of brain death and obtained the following results. 1. The average volume and time required to induce brain death was 4.8$\pm$1.0ml and 143.0$\pm$30.9minutes respectively. 2. There was a steady rise of the ICP after starting the constant infusion of saline, and ICP rised continuously until the brain death (122.0$\pm$62.5mmHg). After reaching to the maximal value (125.0$\pm$47.7mmHg) at 30 minutes after brain death, the ICP dropped and remained approximately constant at the slightly higher level than the mean arterial pressure (MAP). 3. MAP showed no change until the establishment of brain death and it declined gradually. The peak heart rate reached to 172.6$\pm$35.3/min at 30 minutes after the brain death. 4. Even though the body temperature and all hemodynamic variables, such as cardiac output, mean pulmonary arterial pressure, left ventricular (LV) end-diastolic pressure and LV maximum + dp/dt, were slightly greater than those of basal state, at the point of brain death, there was no statistically significant change during t e process of brain death. 5. There was no remarkable arrhythmias during the experiment except ventricular premature beats which was observed transiently in one dog at the time of brain death. Hemodynamic changes in the brain death model induced by gradual ICP increment were inconspicuous, and arrhythmias were rarely seen. Hyperdynamic state, which was observed at the point of brain death in another brain death model caused by abrupt ICP increase, was not observed.

• Journal of Life Science
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• v.19 no.11
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• pp.1568-1574
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• 2009

The purpose of this study was to investigate whether group III muscle afferents play an important role eliciting abnormal blood pressure response mediated during passive muscle stretch in prehypertensive individuals. Eleven middle-aged prehypertensive men (average BP 133/80 mmHg) and nine middle-aged normotensive men (average BP 119/74 mmHg) participated in this study. After 1 min rest baseline data collection, the subject's foot was flexed (dorsiflexion) by an automated cybex for one minute. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), heart rate, stroke volume, cardiac output, and total peripheral resistance were continuously measured on a beat-by-beat basis from a finger via a Finapres device for 1 minute. To evaluate the role of mechanoreflex, a component of exercise pressor reflex, SBP, DBP, and MAP responses over the course of time were examined. The results showed that the pressor response mediated by the muscle mechanoreflex was faster in prehypertensive individuals compared to the normotensive individuals. The substantial pressor response was observed within mean 20 sec of the onset of passive stretch in prehypertension, while mean 45 sec in normotension (p<0.05). It is concluded that excessive pressor response produced during exercise in prehypertension may be due to the dysfunction of the mechano-receptors.

• Journal of Dental Anesthesia and Pain Medicine
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• v.19 no.6
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• pp.353-360
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• 2019

Background: Controlled hypotension (CH) provides a better surgical environment and reduces operative time. However, there are some risks related to organ hypoperfusion. The EV1000/FloTrac system can provide continuous cardiac output monitoring without the insertion of pulmonary arterial catheter. The present study investigated the efficacy of this device in double jaw surgery under CH. Methods: We retrospectively reviewed the medical records of patients who underwent double jaw surgery between 2010 and 2015. Patients were administered conventional general anesthesia with desflurane; CH was performed with remifentanil infusion and monitored with an invasive radial arterial pressure monitor or the EV1000/FloTrac system. We allocated the patients into two groups, namely an A-line group and an EV1000 group, according to the monitoring methods used, and the study variables were compared. Results: Eighty-five patients were reviewed. The A-line group reported a higher number of failed CH (P = 0.005). A significant correlation was found between preoperative hemoglobin and intraoperative packed red blood cell transfusion (r = 0.525; P < 0.001). In the EV1000 group, the mean arterial pressure (MAP) was significantly lower 2 h after CH (P = 0.014), and the cardiac index significantly decreased 1 h after CH (P = 0.001) and 2 h after CH (P = 0.007). Moreover, venous oxygen saturation (ScVO₂) decreased significantly at both 1 h (P = 0.002) and 2 h after CH (P = 0.029); however, these values were within normal limits. Conclusion: The EV1000 group reported a lower failure rate of CH than the A-line group. However, EV1000/FloTrac monitoring did not present with any specific advantage over the conventional arterial line monitoring when CH was performed with the same protocol and same mean blood pressure. Preoperative anemia treatment will be helpful to decrease intraoperative transfusion. Furthermore, ScVO₂ monitoring did not present with sufficient benefits over the risk and cost.

• Journal of Trauma and Injury
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• v.33 no.1
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• pp.38-42
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• 2020

Purpose: Immediate post-laparotomy hypotension (PLH) is a precipitous drop in blood pressure caused by a sudden release of abdominal tamponade after laparotomy in cases of severe hemoperitoneum. The effect of laparotomy on blood pressure in patients with significant hemoperitoneum is unknown. Methods: In total, 163 patients underwent laparotomy for trauma from January 1, 2013 to December 31, 2015. Exclusion criteria included the following: negative laparotomy, only a hollow viscous injury, and hemoperitoneum <1,000 mL. After applying those criteria, 62 patients were enrolled in this retrospective review. PLH was defined as a decrease in the mean arterial pressure (MAP) ≥10 mmHg within 10 minutes after laparotomy. Results: The mean estimated hemoperitoneum was 3,516 mL. The incidence of PLH was 23% (14 of 62 patients). The MAP did not show significant differences before and after laparotomy (5 minutes post-laparotomy, 67.5±16.5 vs. 68.3±18.8 mmHg; p=0.7; 10 minutes post-laparotomy, 67.5±16.5 vs. 70.4±18.8 mmHg; p=0.193). The overall in-hospital mortality was 24% (15 of 62 patients). Mortality was not significantly higher in the PLH group (two of 14 [14.3%] vs. 13 of 48 [27.1%]; p=0.33). No statistically significant between-group differences were observed in the intensive care unit and hospital stay. Conclusions: PLH may be less frequent and less devastating than it is often considered. Surgical hemostasis during laparotomy is important. Laparotomy with adequate resuscitation may explain the equivalent outcomes in the two groups.

• The Korean Journal of Physiology
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• v.15 no.2
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• pp.103-109
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• 1981

In order to determine the dose-response relationship of ethanol on blood pressure and renal function, 2 doses of ethanol were intubated into albino rats. For a direct measurement of arterial blood pressure, a polyethylene catheter(PE 10) was implanted in the abdominal aorta, and the other end of the catheter was pulled out of the back of the neck. The experiment was conducted after the rats recovered from the surgery. After emptying their bladders, the rats were placed in a metabolism cage. Mean arterial pressure (MAP) was measured and arterial blood samples were collected through the catheter. Following the collection of the control urine sample, 1 ml of 10 g% (low dose), or 30 g% (high dose) of ethanol/100 g BW was intubated. 1 ml of water/100 g BW was intubated into the control group. MAP and blood samples were taken every hour, and urine samples were collected every 90 min for 3 hours. Blood alcohol concentrations reached a peak at 1 hour (low dose: $105.0{\pm}7.5$, high dose: $214.7{\pm}20.2\;mg%$) and decreased linearly thereafter. Following alcohol ingestion, MAP began to decrease at 15 min and remained at a significantly low level thoughout the 3 hours experimental period(low dose: $112{\pm}2{\rightarrow}102{\pm}4$, high dose: $117{\pm}2{\rightarrow}100{\pm}8\;mmHg$). Urine Flow increased markedly during the first 90 min of ethanol ingestion (low dose: $0.88{\pm}0.20{\rightarrow}1.04{\pm}0.22$, high dose: $0.56{\pm}0.11{\rightarrow}1.35{\pm}0.18\;ml/1.5\;hr$) and decreased during the second 90 min period(low dose: $0.25{\pm}0.06$, high dose: $0.22{\pm}0.06\;ml/1.5\;hr$). Urine flow of the control group decreased gradually during the experiment $(0.88{\pm}0.10{\longrightarrow}0.59{\pm}0.09{\rightarrow}0.45{\pm}0.09\;ml/1.5\;hr)$. These results indicate that the blood-pressure-lowering and diuretic effects of ethanol are dose-related: higher doses of ethanol produce a greater decrease in blood pressure and greater diuresis.

• Biomolecules & Therapeutics
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• v.8 no.4
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• pp.325-331
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• 2000

The present study was designed to assess the role of spinal adenosine $A_2$ receptor in the regulation of cardiovascular functions such as mean arterial pressure (MAP) and heart rate (HR) in male Sprague-Dawley rats. Rats (250~300 g) were anesthetized with urethane and paralyzed with d-tubocurarine and artificially ventilated. blood pressure and HR were continuously monitored via a femoral catheter connected to a pressure transducer and a polygraph. Drugs were administered intrathecally using injection cannula through guide cannula which was inserted inthrathecally at lower thoracic level through a puncture of an atlantooccipital mombrane. Intrathecal injection of an adenosine $A_2$ receptor agonist, 5'-(N-cyclopropyl)-carboxamaidoadenosine (CPCA; 1, 2 and 3 nmol, respectively), produced a dose-dependent decrease in MAP and HR. Pretreatment with $N^{G}$-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor or 10 nmol of MDL-12,330, an adenylate cyclase inhibitor blocked significantly the depressor and bradycardic effect of 2 nmol of CPCA. But, Pretreatment with 3 nmol of bicuculline, gamma-aminobutyric acid A (GAB $A_{A}$) receptor antagonist, or 50 nmol of 5-aminovaleric acid, GAB $A_{B}$ receptor antagonist did not inhibit the depressor and bradycardic effect of 2 nmol of CPCA. These results indicate that adenosine $A_2$ receptor in the spinal cord plays an inhibitory role in the regulation of cardiovascular function and that the depressor and bradycardic action of adonosine $A_2$ receptor are mediated via the synthesis of nitric oxide and the activation of adenylate cyclase in the spinal cord of rats.s.s.s.