• Advances in Traditional Medicine
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• v.7 no.4
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• pp.409-417
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• 2007

We investigated the effect of Arogh, a polyherbal formulation (PHF) on animal models of anxiety based on exploratory behavior. The anxiolytic activity of polyherbal formulation (30, 100, 300 and 500 mg/kg) was studied using various behavioural paradigms such as elevated plus maze (EPM), light/dark apparatus (LDA), open field apparatus (OFA), hole board apparatus (HBA). Diazepam (1 mg/kg) was used as a standard anxiolytic drug. The effect of PHF (100 and 300 mg/kg) on serotonin, dopamine and noradrenaline mediated behaviour was studied by lithium induced head twitches in rats, haloperidol induced catalepsy in mice and clonidine induced hypothermia in rats respectively. In EPM, PHF (100, 300 and 500 mg/kg) significantly (P < 0.05) increased the time spent in open arms and the number of entries in open arms. In LDA, PHF (100, 300 and 500 mg/kg) significantly (P < 0.05) increased the time spent in lit zone. In OFA, PHF (100, 300 and 500 mg/kg) significantly (P < 0.05) increased the number of assisted rearing and the number of squares traversed. In HBA, PHF (100, 300 and 500 mg/kg) significantly (P < 0.05) increased the number of head poking. In lithium induced head twitches, PHF (100 and 300 mg/kg) significantly (P < 0.05) decreased the number of head twitches. In haloperidol induced catalepsy, PHF (300 mg/kg) decreased the duration of catalepsy significantly (P < 0.05) at 60 min. In clonidine-induced hypothermia, PHF (300 mg/kg) did not modify the effect. Drugs must be carefully assessed on EPM test and therefore in the present study EPM is supported by other tests. Present study indicates that Arogh, a polyherbal formulation possess anxiolytic activity. It diminished serotonergic transmission and decreased the duration of catalepsy indicating potentiation of dopaminergic transmission. Thus, Arogh a polyherbal formulation contains bioactive principles which possess anxiolytic activity and modified 5-HT and DA mediated behaviour.

• Journal of Veterinary Science
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• v.24 no.1
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• pp.2.1-2.14
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• 2023

Background: Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear. Objectives: This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms. Methods: In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4℃) for three hours per day for three weeks. Results: CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia. Conclusions: These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.

• Journal of Chest Surgery
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• v.27 no.10
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• pp.854-857
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• 1994

Hypothermia and circulatory arrest is efficatious adjunct in the surgical treatment of conventionally difficult or otherwise inoperable lesion. This technique was utilized in 5 patients, 3 with membraneous obstruction of inferior vena cava[MOVC] and 1 with giant middle cerebral artery aneurysm and 1 with renal cell carcinoma invading inferior vena cava. All membraneous obstruction of inferior vena cava patients had excellent results but the others died of operative complications. The rationale for the use of complete cardiac arrest with hypothermia is reviewed and the use of these technique in selected patients is warrented.

• Journal of Chest Surgery
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• v.2 no.1
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• pp.85-104
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• 1969

This experiment was carried out to study the effect of rapid hemorrhage on cardiopulmonary hemodynamics of the cooled dogs. Hypothermia was induced by means of body surface cooling with ice water. Lowest esophageal temperatures ranged from 24 to 26 degree. Dogs were bled via the femoral artery into a reservoir in amount of the equivalent blood volume of 3% of body weight of the dogs. Some dogs were reinfused with the same amount of blood which they lost and others infused with 5% dextrose solution. Fourty adult mongrel dogs were divided into three groups: group I[15 dogs]; dogs were bled in normothermic state. Five dogs had no further treatment, but five dogs were reinfused with blood and five infused with 5% dextrose solution 30 minutes after bleeding. GroupII[10 dogs]; dogs were bled as group I after having been cooled. Five dogs were reinfused with blood as group I. Group III[15 dogs]; dogs were first bled and then cooled. Reinfusion procedures were the same as in group l Results were as follow: 1. The heart rate showed a slight decrease after bleeding in group I and then increased over the control level after 60 minutes. After reinfusion and infusion, the heart rate was also increased gradually and after three hours almost returned to the control level. In group II and groupIll, the heart rate decreased remarkably and after reinfusion showed a light increase but after infusion tended to decrease cotinually. 2. The stroke volume showed remarkable decrease after bleeding in group I., and recovered to control level after reinfusion and infusion,and then gradually decreased again. In group III, the stroke volume showed no remarkable change after hypothermia, and tended to decrease after reinfusion. In group III, the stroke volume decreased remarkably after bleeding and hypothermia,and clearly increased after reinfusion and infusion and then returned to control level. 3. Femoral mean pressure declined very rapidly and significantly right after bleeding and showed a remarkable prompt rise after reinfusion and infusion in group I [67% recovery]. On the other hand, it declined remarkably after hypothermia and bleeding and showed a slight rise after reinfusion and infusion in group II[46% recovery] and III [41% recovery]. 4. Venous pressure declined slightly after bleeding and tended to return to the control level after reinfusion and infusion,in group I. In group II, it did not change significantly during hypothermia but showed a slight decline after bleeding and returned toward control level after reinfusion. In group III, it declined slightly after bleeding and showed no significant change after hypothermia and rose over the control level after reinfusion and infusion. 5. Right ventricular systolic pressure decreased markedly after bleeding and then increased progressively after 30 minutes. It increased after reinfusion and infusion as well, approaching the control level in group I. In group II, it showed no significant change during hypothermia, but decreased remarkably after bleeding and then returned to near control level after reinfusion. In group III, it was decreased markedly after bleeding but did not change significantly during hypothermia and showed a slight increase after reinfusion. 6. The respiratory rate increased gradually after bleeding and decreased gradually after reinfusion but did not return to the control level, whereas it decreased near to the control level after infusion,and tended to increase in group I. In group II, it decreased significantly after hypothermia and bleeding but returned near to the control level after reinfusion. In group III, it showed a remarkable decrease after hypothermia and increased slightly after reinfusion and infusion but did not returned to the control level. In group I, the tidal volume decreased slightly after hemorrhage, and increased gradually to near the control level after 3 hours following reinfusion.

• Journal of Chest Surgery
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• v.29 no.1
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• pp.14-23
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• 1996

Circulatory arrest under deep hypothermia is an important auxiliary means for cardiac surgery, especially useful in pediatric patients. However, its clinical safety, particularly with regard to the neurologic outcome after long duration of circulatory arrest, is still not established. This study is a review of the eight years'clinical experience of hypothermic circulatory arrest at the Seoul national University Children's Hospital. During an eight-year period from January 1986 through December 1993, a total of 589 consecutive cardiac operations were done using circulatory arrest under deep hypothermia. Among them, 434 consecutive patients, in whom the duration of arrest was 20 minutes or more, are the subject of this study. The duration of arrest ranged from 20 minutes to 82 minutes (mean = 38.7 minutes) under rectal temperature in the range from 12.5$^{\circ}C$ to 25.8$^{\circ}C$. Early neurologic abnormalities occurred in 47 patients : seizure attacks in 28 patients, motor paralyses with or w thout seizure in 12, blindness in 2, and no recovery of consciousness in 5 patients. The rate of incidence of early neurologic abnormalities was calculated at 15.7%. 25 patients showed late neuropsychologic sequelae, such as motor paralysis (9 patients), recurrent seizures (6), developmental delay (8), and definitely low intelligence (2). The rate of incidence of late neurologic sequelae was 8.5%, By statistical analysis, the following factors were identified as the risk factors for post-arrest neurologic abnormalities ; 1) long duration of circulatory arrest, 2) lower-than-ideal body weight, 3) preexisting neurological abnormalities, 4) associated non-cardiovascular congenital anouialies, and 5) low blood pressure during the early post-arrest period. It is concluded that circulatory arrest under deep hypothermia is a relatively safe means for pediatric cardiac surgery with acceptable risk. However, to warrant maximal safety, it is desirable to limit the duration of arrest to less th n 40 minutes. In addition, it is our contention that the early post-arrest period is a very critical period during which maintenance of adequate perfusion pressure in important for the neurologic outcome.

• Journal of Chest Surgery
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• v.34 no.6
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• pp.465-471
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• 2001

Background: Hypothermia protects the brain by suppressing the cerebral metabolism and it is performed well enough before the total circulatory arrest(TCA) in the operation of aortic disease. Generally, TCA has been performed depending on the rectal or nasopharyngeal temperatures; however, there is no definite range of optimal temperature for TCA or an objective indicator determining the temperature for safe TCA. In this study, we tried to determine the optimal range of temperature for safe hypothermic circulatory arrest by using the intraoperative electroencephalogram(EEG), and studied the role of EEG as an indicator of optimal hypothermia. Material and Method: Between March, 1999 and August 31, 2000, 27 patients underwent graft replacement of the part of thoracic aorta using hypothermia and TCA with intraoperative EEG. The rectal and nasopharyngeal temperatures were monitored continuously from the time of anesthetic induction and the EEG was recorded with a ten-channel portable electroencephalography from the time of anesthetic induction to electrocerebral silence(ECS). Result: On ECS, the rectal and nasopharyngeal temperatures were not consistent but variable(rectal 11$^{\circ}C$ -$25^{\circ}C$, nasopharynx 7.7$^{\circ}C$ -23$^{\circ}C$). The correlation between two temperatures was not significant(p=0.171). The cooling time from the start of cardiopulmonary bypass to ECS was also variable(25-127min), but correlated with the body surface area(p=0.027). Conclusion: We have found that ECS appeared at various body temperatures, and thus, the use of rectal or nasopharyngeal temperature were not useful in identifying ECS. Conclusively, we can not fully assure cerebral protection during hypothermic circulatory arrest in regards to the body temperatures, and therefore, the intraoperative EEG is one of the necessary methods for determining the range of optimal hypothermia for safe circulatory arrest. :

• Journal of Oriental Neuropsychiatry
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• v.16 no.1
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• pp.171-183
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• 2005

Objective : The Korean famous medicinal prescription of Subi-jeon was investigated for their antidepressant effects by tail suspension test, hot plate test, reserpine-induced hypothermia test. In addition, the monoamine oxidase activity was determined in vivo. Methods : The methanol extract reduced dose-dependently the duration of immobility in the tail suspension test, by 31.4 and 34%(p<0.05) at doses of 500mg/kg and 1g/kg, respectively, compared with control group. In comparison with this, the effect of the water extract was very weak. Results : 1. In the hot plate test, the methanol extract potently increased the jump latency time(p<0.05) compared to the control group, exhibiting the inhibition rate of 197% and 256% at doses of 500mg/kg and 1g/kg(per os), respectively, which is more effective than the water extract. 2. Both extracts suppressed the fall of body temperature induced by reserpine(reserpine-induced hypothermia) in a dose-dependent manner, showing the less effect at lower doses and better effect at higher doses compared to the water extract. 3. Both extracts inhibited the brain monoamine oxidase activity in an in vivo assay compared to the control group, the activity of water extract was better than that of the methanol extract. Conclusion : The prescription of Subi-jeon can be useful for the prevention and treatment of depression.

• Journal of Chest Surgery
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• v.41 no.4
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• pp.405-416
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• 2008

Background: Spinal cord ischemic injury during thoracic and thoracoabdominal aortic surgeries remains a potentially devastating outcome despite using various methods of protection. Neuronal voltage-dependent sodium channel antagonists are known to provide neuroprotection in cerebral ischemic models. This study was designed to compare the neuroprotective effects of phenytoin with those of hypothermia in a rabbit model of spinal cord ischemia. Material and Method: Spinal cord ischemia was induced in New Zealand white rabbits by means of infrarenal aortic cross clamping for 25 minutes. Four groups of 8 animals each were studied. The control group and the hypothermia group received retrograde infusion of saline only ($22^{\circ}C$, 2 mL/min); the normothermic phenytoin group and the hypothermicphenytoin group received retrograde infusion of 100 mg of phenytoin at different rectal temperatures ($39^{\circ}C$ and $37^{\circ}C$, respectively) during the ischemic period. The neurologic function was assessed at 24 and 72 hours after the operation with using the modified Tarlov criteria. The spinal cords were harvested after the final neurologic examination for histopathological examination to objectively quantify the amount of neuronal damage. Result: No major adverse effects were observed with the retrograde phenytoin infusion during the aortic ischemic period. All the control rabbits became severely paraplegic, Both the phenytoin group and the hypothermia group had a better neurological status than did the control group (p < 0.05). The typical morphological changes that are characteristic of neuronal necrosis in the gray matter of the control animals were demonstrated by means of the histopathological examination, whereas phenytoin or hypothermia prevented or attenuated these necrotic phenomena (p < 0.05). The number of motor neuron cells positive for TUNEL staining was significantly reduced, to a similar extent, in the rabbits treated with phenytoin or hypothermia. Phenytoin and hypothermia had some additive neuroprotective effect, but there was no statistical significance between the two on the neurological and histopathological analysis. Conclusion: The neurological and histopathological analysis consistently demonstrated that both phenytoin and hypothermia may afford significant spinal cord protection to a similar extent during spinal cord ischemia in rabbits, although no significant additive effects were noticed.

• Proceedings of the KAIS Fall Conference
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• 2011.12a
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• pp.170-173
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• 2011

Therapeutic hypothermia(TH) improves neurological outcomes and reduces mortality among survivors of out-of-hospital cardiac arrest. Animal and human studies have shown that TH results in improved salvage of the myocardium, reduced infarct size, reduced left ventricular remodeling and better long-term left ventricular function in settings of regional myocardial ischemia. This study is to investigate the effect of TH on post-resuscitation myocardial dysfunction and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction (MI). Thoracotomies were performed in 10 Male Sprague-Dawley rats weighing 450-550 g. MI was induced by ligation of the left anterior descending coronary artery (LAD). Ninety min after LAD ligation, ventricular fibrillation induction and subsequent cardiopulmonary resuscitation was performed before defibrillation attempts. Animals were randomized to two groups: a) Acute MI-Normothermia b) Acute MI-Hypothermia ($32^{\circ}C$ for 4 h). Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured echocardiographically together with duration of survival. Ejection fraction, cardiac output and myocardial performance index were $54.74{\pm}9.16$, $89.00{\pm}8.89$, $1.30{\pm}0.09$ respectively and significantly better in the TH group than those of the normothermic group at the first 4 h after resuscitation($32.20{\pm}1.85$,$41.60{\pm}8.62$,$1.77{\pm}0.19$)(p=0.00). The survival time of the hypothermic group ($31.8{\pm}14.8$ h) was greater than that of the normothermic group($12.3{\pm}6.5$ h, p<0.05). This study suggested that TH attenuated post resuscitation myocardial dysfunction in acute MI and would be a potential strategy in post resuscitation care.

• The Korean Journal of Pharmacology
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• v.5 no.2
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• pp.93-103
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• 1969

Saponin, essential oil, fat oil and alkaloidal fraction were fractionated from the ethanol extract of fanax ginseng. Effect of each fraction of Panax ginseng upon the temperature response induced by reserpine, chlorpromazine and nembutal was investigated in mice, so as to secure some hidden facets of each fraction of Panax ginseng acting upon central nervous system. The authors could arrive at some results, that is: (1) Inhibitory effect of Panax ginseng upon temperature decline induced by nembutal and chlorpromazine and potentiating action upon hyperthermia induced by reserpine reside mainly in saponin fraction and slightly in essential oil fraction. (2) The effect of Ginseng saponin on temperature response in nice seems to be related with the liberation of serotonin and histamine.