• Advances in Traditional Medicine
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• v.4 no.2
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• pp.95-99
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• 2004

The ethanolic extract of some medicinal plants having anti-asthmatic activity such as Solanum xanthocarpum, Curcuma longa, Glycyrrhiza glabra, Piper longum, A. vasica, A. lebbeck, and Tinospora cordifolia was evaluated for antihistaminic and anti-cataleptic activity. The aqueous solution of ethanolic extract of S. xanthocarpum and G. glabra potentiated histamine-induced tracheal chain contractions. Whereas, C. longa, P. longum, and T. cordifolia, and A. lebbeck were without any significant effect on histamine. Only A. vasica inhibited histamine-induced tracheal chain contraction. G. glabra per se produced contraction of the tracheal chain, which was blocked by pretreatment with atropine. Single dose of S. xanthocarpum potentiated clonidine-induced catalepsy but on repeated doses (once in a day for 3 days) inhibited catalepsy. Pretreatment with ethanolic extract of C. longa, P. longum, T. cordifolia inhibited catalepsy whereas G. glabra and A. lebbeck significantly potentiated clonidine-induced catalepsy. None of the extracts inhibited haloperidol-induced catalepsy. Thus the extracts having antihistaminic activity or mast cell stabilizing activity inhibited clonidineinduced catalepsy.

• Journal of fish pathology
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• v.9 no.1
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• pp.41-51
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• 1996

The present study was undertaken to investigate the physiological characteristics of the adrenergic responses in the tilapia dorsal aorta. Epinephrine, norepinephrine, clonidine and methoxamine in the presence of propranolol($3{\times}10^{-6}$M), induced only endothelium-independent and concentration-dependent vasocontractions in tilapia dorsal aorta. The rank order of potency of adrenergic agonists inducing vasocontraction was epinephrine>norepinephrine>phenylephrine>clonidine>ethoxamine, Yohimbine produced a parallel shift of the concentration-vascontraction curves of epinephrine, norepinephrine, phenylephrine and clonidine to the right, while prazosin depressed the maximum responses of epinephrine and norepinephrine. Calcium-free physiological solution and verapamil markedly reduced epinephrine or norepinephrine-induced vasocontractions. These results suggest that a-adrenergic agonists produce only on endothelium-inedpenent casoconstrictions in tilapia dorsal aorta and these effect of a-adrenergic agonists, which might be associated with both calcium release from intracellular stores and calcium influx through voltage-dependent calcium channel.

• The Korean Journal of Pain
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• v.9 no.1
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• pp.159-165
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• 1996

Background: Epidural analgesia has been widely used for postoperative pain relief. However, it is not known which regimen provides the best result due to many variety. The aim of this study is to evaluate the analgesia and side effects of epidural mixute of fentanyl, bupivacaine and clonidine, as one kind of regimen. Methods: One hundred adult patients scheduled for upper abdominal surgery under general anesthesia were evaluated. Epidural catheterization was done after operation. A bolus, 0.1% bupivacaine 10 ml containing fentanlyl 100 ${\mu}g$, was administered and followed up with continuous infusion of mixture of fntanyl 600 ${\mu}g$, 0.5% bupivacaine 20ml and clonidine 150 ${\mu}g$ at a rate of 2ml/hr for 50 hours. Analgesia was assessed using VAS, PHS and PRS. Side effects and number of patients who took additional analgesics were evalutated. Plasma samples were obtained to determine fentanyl concentration. Results: After the administrations of drugs, patients pain scores decreased notably, and pain relief scores increased significantly. Minimum side effects were noted. Twenty-one patients required additional analgesics. Plasma concentration of fentanyl was 0.07~0.14 ng/ml. Conclusion: Epidural infusion of mixture of fentanyl, bupivacaine and clonidine is an effective regimen for postoperative pain relief after upper abdominal surgery.

• Korean Journal of Veterinary Research
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• v.28 no.1
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• pp.29-36
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• 1988

To examine the selectivity of verapamil, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor rsponses, effects of verapamil on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits, spinal rabbits, rats and pithed rats. To evaluate the effects of verapamil on each pressor response induced by norepinephrine, phenylephrine and clonidine, these agonists were previously injected into a ear vein, and then same procedures were performed 1~2 min after treatment with intravenous verapamil. The results are summarized as follows: 1. Intravenous verapamil produced dose-dependent depressor response in rabbits and rats. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylphrine($30{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 3. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$), phenylephrine($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. 4. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$) and phenylephrine($10{\mu}g/kg$) were inhibited by pretreatment with intravenous verapairlil in rats and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 5. Pressor responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine($30{\mu}g/kg$) and clonidine($100{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in pithed rats. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that verapamil significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors and the inhibition is greater in alpha-2 adrenoceptor-induced response than in alpha-1 adrenoceptor-induced one, and calcium channel takes part in the process of the pressor response mediated by alpha-1 adrenoceptors as well as alpha-2 adrenoceptors.

• The Korean Journal of Pharmacology
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• v.23 no.2
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• pp.87-94
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• 1987

The role of central adrenergic activity in the genesis of stress ulcers was investigated by intracerebroventricular (i.c.v.) administration of catecholamines and clonidine in pylorus-ligated rats restrained for 4 hours at a temperature of $4^{\circ}C$. 1. The stress-induced ulceration was markedly decreased by the i.c.v. administration of norepinephrine, epinephrine, dopamine or low dose of clonidine. 2. After an i.c.v. administration of norepinephrine or epinephrine, the volume of gastric juice, and both acid and pepsin secretion were markedly decreased. 3. Dopamine or a low dose of clonidne decreased the volume of gastric juice and acid secretion but did not affect pepsin secretion. 4. Isoproterenol caused a decrease in the volume of gastric juice and acid secretion, however, the ulcerogenesis was similar to that of the control. 5. Gastric function as well as ulcerogenesis was little affected by a high dose of clonidine. From the above results, it is suggested that central adrenergic activation inhibits cold-restraint induced ulcerogenesis via adrenergic alpha and dopaminergic receptors, and that this effect may be mediated by a decrease in gastric acid secretion. It is also suggested that other factors may be involved in this antiulcerogenic effect.

• The Korean Journal of Pharmacology
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• v.21 no.2
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• pp.90-98
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• 1985

1) In the study of the forced-swimming test in mice (FSM), the duration of immobility posture was dose-dependently shortened by ${\alpha}_2$-agonists, clonidine and guanabenz. BH-T 933 and oxymetazoline also decreased it . Xylazine rather increased the immobility duration at low dose. 2) ${\alpha}_1$-Agonists, cirazoline, amidephrine and methoxamine, however, showed inconsistent effect on the immobility duration (ID). 3) The decrease in ID by clonidine and guanabenz was antagonized by pretreatment with yohimbine, idazoxan and phentolamine (${\alpha}_2$antagonist), but not by prazosin and corynanthine (${\alpha}_1$-antagonist) .4) The ID in the FSM was shortened dose-dependently by d-amphetamine, and it was also antagonized by yohimbine, but not by prazosin. 5) In the mice pretreated with either ${\alpha}$-methyl-p-tyrosine or reserpine, or with combination of both, the decrease in ID was still evoked by clonidine. 6) When the mice were chronically treated with antidepressants (desipramine and imipramine), or with electroconvulsive shock, clonidine still decreased the ID as it did in the control. 7) These results provided the evidences to hypothesize that the change of the ID in the FSM is closely related with the postsynaptie ${\alpha}_2$-adrenoceptor located on the central noradrenergic neuron body. Furthermore, it is assumed that this escape-directed behavior enhanced by ${\alpha}_2$-adrenoceptor agonist may be the result in some analogy with the incentive of drives which are directed toward the self-preservation.

• Korean Journal of Veterinary Research
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• v.28 no.1
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• pp.23-28
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• 1988

To examine the selectivity of diltiazem, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor responses, effect of diltiazem on alpha-adrenocepter agonist-induced pressor responses were investigated in urethane-anesthetized rabbits and spinal rabbits. The results are summarized as follows: 1. Intravenous diltiazem(10, 30, 100, 300, $1000{\mu}g/kg$) produced dose-dependent depressor response in rabbits. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylephrine ($30{\mu}g/kg$) were inhibited by pretreatment with intravenous diltiazem in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by diltiazem. 3. Presser responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine ($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous diltiazem in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by diltiazem. The inhibition of clonidine-induced pressor response by diltiazem was slightly prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that diltiazem significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors.

• YAKHAK HOEJI
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• v.28 no.6
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• pp.305-311
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• 1984

Relationship between hypertension and monoamine oxidase (MAO) activity in rat brain and the change of this relationship by presynaptic ${\alpha}-receptor$ agonist were studied. Animals were divided into three groups. Group I was composed of normotensive Sprague-Dawley rats (NR), group II of spontaneously hypertensive rats (SHR) and group III of acquired hypertensive rats induced by deoxycorticosterone acetate (DOCA) and NaCl treatment. Clonidine, a presynaptic ${\alpha}-receptor$ agonist, was administered to groups II and III. Blood pressures and MAO activities were measured in each group. MAO activities in the brain of SHR were lower than those of NR. Animals in group II received clonidine which lowered blood pressures but did not change MAO activities in the brain. DOCA and NaCl induced hypertension 21 days after these treatments in group III and did not cause any changes in brain MAO activity. Clonidine lowered blood pressures of group III but did not change MAO activities. The data from the present study suggest that abnormaly low MAO activities in SHR brain may be one of the underlying factors for the susceptibility to hypertension and that the decrease in noradrenergic neuronal activities through presynaptic ${\alpha}-receptor$ activation by clonidine may not be related to the changes of brain MAO activities.

• YAKHAK HOEJI
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• v.33 no.6
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• pp.333-338
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• 1989

It has been postulated that abnormal characteristics of central noradrenergic nervous system has been implicated in the development and maintenance of hypertension in several modes of experimental hypertension including spontaneously hypertensive rats (SHR). In the present study, we attempt to determine if abnormal characteristics of central noradrenergic nervous system in SHR is caused by genetic factors or hypertensive phenomena by evaluating the changes of central adrenoceptors after long-term treatment of clonidine. Animals were divided into three groups; (1) 14 week-old SHR; (2) age-matched normotensive Wistar rats (NW); (3) DOCA-Salt induced hypertensive rats (DS). Clonidine (100 ug/kg) or vehicle was injected intraperitonealy twice a day for 15 days. Changes of ${\alpha}_1-$ and ${\alpha}_2-receptor$ desities following clonidine treatment were determiend in frontal corte, medulla oblongata and hypothalamus using 3H-WB4101 and 3H-clonidine, respectively. Densities of ${\alpha}_1$ and ${\alpha}_2-receptors$ following clonidine treatment were not changed in frontal cortex and medulla oblongate of SHR as well as DS, but increased in frontal cortex of NW and decreased in medulla oblongata of NW. On the other hand, densities of ${\alpha}_1-receptors$ were increased and densities of ${\alpha}_2-receptors$ were not changed in hypothalamus of SHR but densities of ${\alpha}_1-$ and ${\alpha}_2-receptors$ were decreased in hypothalamus of DS as well as NW. These results suggest that such differences in frontal cortex and medulla oblongata of SHR may be results of hypertensive phenomena whereas those in hypothalamus may be relevant to genetic factors of SHR.

• The Korean Journal of Pain
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• v.36 no.2
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• pp.216-229
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• 2023

Background: The role of the sympathetic nervous system appears to be central in causing pain in complex regional pain syndrome (CRPS). The stellate ganglion block (SGB) using additives with local anesthetics is an established treatment modality. However, literature is sparse in support of selective benefits of different additives for SGB. Hence, the authors aimed to compare the efficacy and safety of clonidine with methylprednisolone as additives to ropivacaine in the SGB for treatment of CRPS. Methods: A prospective randomized single blinded study (the investigator blinded to the study groups) was conducted among patients with CRPS-I of the upper limb, aged 18-70 years with American Society of Anaesthesiologists physical status I-III. Clonidine (15 ㎍) and methylprednisolone (40 mg) were compared as additives to 0.25% ropivacaine (5 mL) for SGB. After medical treatment for two weeks, patients in each of the two groups were given seven ultrasound guided SGBs on alternate days. Results: There was no significant difference between the two groups with respect to visual analogue scale score, edema, or overall patient satisfaction. After 1.5 months follow-up, however, the group that received methylprednisolone had better improvement in range of motion. No significant side effects were seen with either drug. Conclusions: The use of additives, both methylprednisolone and clonidine, is safe and effective for the SGB in CRPS. The significantly better improvement in joint mobility with methylprednisolone suggests that it should be considered promising as an additive to local anaesthetics when joint mobility is the concern.