• 대한수의학회지
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• 제37권2호
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• pp.331-338
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• 1997

최근 동물의 진통 및 진정을 목적으로 널리 사용되고 있는 imidazole 유도체인 clonidine, medetomidine, etomidate 등의 약물과 xylazine의 효과를 발정정지기의 척출 돼지 자궁근에서 검토하였다. Clonidine($10^{-8}{\sim}10^{-6}M$)이나 medetomidine($10^{-8}{\sim}10^{-6}M$)은 xylazine과 비슷한 정도로 용량의존적인 자궁근의 수축을 일으켰다. Clonidine, medetomidine, xylazine 등의 $EC_{50}$는 각각 24.7nM, 19.9nM, 45.1nM이었다. 그러나 etomidate는 $10^{-6}M$ 미만의 농도에서 반응이 거의 없었으며, $10^{-6}M$ 이상에서 수축반응을 일으켰다. 이들 agonists의 효과는 yohimbine($10^{-8}{\sim}10^{-6}M$), idazoxan($10^{-7}{\sim}10^{-5}M$), tolazoline($10^{-7}{\sim}10^{-5}M$) 등의 ${\alpha}_2-adrenoceptor$ antagonists에 의해서 차단되었으나, ${\alpha}_1-adrenoceptor$ antagonist인 prazosin ($10^{-6}M$)에 의해서는 차단되지 않았다. 또한 $Ca^{2+}-free$ medium이나 verapamil($10^{-5}M$)의 전처치에 의해서 이들 agonist의 효과가 완전히 차단되었다. 결론적으로 발정정지기의 돼지 자궁근에서 clonidine, medetomidine, etomidate, xylazine 등은 ${\alpha}_2-adrenoceptors$의 흥분을 통해 자궁근의 수축을 일으키며, 이 효과는 voltage-dependent $Ca^{2+}$ channels을 통한 extracellular $Ca^{2+}$ influx의 증가에 의한 것으로 추론하였다.

• 대한수의학회지
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• 제34권3호
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• pp.479-486
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• 1994

Effects of catecholamines and the site of receptor of catecholamines were investigated in the longitudinal muscle of the rumen. In order to this experiment, specimens were obtained from 35 Korean Native Cattles, 2-3 years old, in the Kwang-ju area slaughterhouse. Longitudinal muscle strips of rumen were made from sample, and then measured the isometric contraction with physiograph in $37{^{\circ}C}$ organ bath. The results were summarized as follows. 1. 30% of all strips showed rhythmic contraction after short incubation time. 2. Relaxation produced by catecholamines in this preparations increased in a dose-dependant manner. 3. Isoproterenol(${\beta}$-agonist) caused relaxation, but phenylephrine(${\alpha}_1$-agonist) and xylazine(${\alpha}_2$-agonist) were unaffected. 4. The relaxation induced by epinephrine and norepinephrine were not affected by phentolamine(${\alpha}$-blocker) and prazosin(${\alpha}_1$-blocker), yohimbine(${\alpha}_2$-blocker). But propranolol(${\beta}$-antagonist) abolished the effect of catecholamines on relaxation. 5. It is concluded that catecholamines produced relaxation in the longitudinal muscle of rumen via the ${\beta}$-adrenoceptor.

• 대한수의학회지
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• 제33권1호
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• pp.71-80
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• 1993

The central nervous system depressant effect of xylazine and xylazine-ketamine was studied in chicken and mice. Intraperitoneal injection of xylazine(1~30 mg/kg) and xylazine(1~30 mg/kg)-ketamine(100 mg/kg) induced a loss of the righting reflex in chicken and mice, respectively. These effects of xylazine were dose-dependent. The results obtained were as follows; 1. The effect of xylazine-induced depression was antagonized by adrenergic antagonists having ${\alpha}_2$-blocking activity(yohimbine, tolazoline, piperoxan and phentolamine). 2. Yohimbine was most effective in the reduction of the CNS depression by xylazine. 3. Phenoxybenzamine and prazosin did not reduced CNS depression by xylazine in both species. 4. Labetalol (${\alpha}_1$, ${\beta}_1$-adrenergic antagonist) and propranolol(${\beta}$-adrenergic blocking agent) were not effective in reducing xylazine induced depression. 5. Cholinergic blocking agents (atropine and mecamylamine), a dopaminergic antagonist (Haloperidol), a histamine $H_1$-antagonist(chlorpheniramine), a histamine $H_2$-antagonist(cimetidine), a serotonergic-histamine $H_1$ antagonist(cyproheptadine) were not effective in reducing xylazine-induced depression. 6. Xylazine-induced depression is mediated by ${\alpha}_2$-adrenergic receptors and appears not to be involved in cholinergic, dopaminergic, serotonergic or histaminergic pathways.

• Archives of Pharmacal Research
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• 제12권4호
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• pp.243-248
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• 1989

Effects of B-HT 920 on the vagally stimulated gastric acid secretion were studied in anesthetized and gastric fistula rats. When the gastric acid secretion was increased by stimulation of the vagus nerve, B-HT 920 was partially attenuated by prazosin, $\alpha_1-$adrenoceptor antagonist and virtually abolished by yohimbine, $\alpha_2-$adrenoceptor antagonist. On the other hand, when the gastric acid secretion was increased by the infusion of bethanechol, a muscarinic parasympathetic stimulant, B-HT 920 had no effect on the bethanechol-induced gastric acid secretion. These results suggest that B-HT 920 inhibits vagally induced gastric acid secretion by activation of presynaptic $\alpha-$adrenoceptors located on the vagally stimulated pathways in the gastric wall and this effect of B-HT 920 is more related to $\alpha_2-$adrenoceptors than $\alpha_1-$adrenoceptors.

• 대한수의학회지
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• 제35권2호
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• pp.255-261
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• 1995

Amitraz frequently causes the side effect of intestinal stasis or bloat in mammals. It is very similar to the side effect of xylazine or clonidine which produce the inhibition of intestinal motility through the stimulation of ${\alpha}_2$ adrenoceptor. Therefore, we examined whether amitraz causes intestinal stasis or bloat through the inhibition of intestinal motility or whether amitraz produces the inhibition of intestinal motility through the stimulation of ${\alpha}_2$ adrenopceptor. Amitraz inhibited the intestinal motility in a dose-dependent manner in isolated rabbit jejunum and isolated pig ileum. These inhibitory effects of amitraz were blocked by yohimbine but not by prazosin. The effect of intestinal contraction of carbachol or high-potassium was not affected by the pretreatment of amitraz. However, the con-traction of histamine was inhibited by the pretreatment of amitraz. It is concluded that amitraz mainly inhibits the intestinal motility through the stimulation of ${\alpha}_2$-adrenoceptor although partially antihistaminic action of amitraz can be involved.

• 대한수의학회지
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• 제39권4호
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• pp.710-714
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• 1999

In veterinary medicine amitraz has been used as an insecticide to eliminate mites, lice, and ticks in dogs, cats, goats, swine and cattle. We performed the experiment on bradycardiac effect of arnitraz in rabbits. Under anesthetized with urethane (1g/kg, 25% w/v, SC), the femoral artery was cannulated by a polyvinyl tube which was connected with pressure transducer for continuous measurement of heart rate. Amitraz (0.5-2.5mg/kg, IV) reduced the heart rate in a dose-dependent manner. Pretreatment of yohimbine (2.0mg/kg) or atropine (2.0mg/kg and 4.0mg/kg) affected the response of amitraz but pretreatment of prazosin (0.5mg/kg) or propranolol (1.0mg/kg) did not. Moreover, the effect of amitraz was blocked by vagotomy. The result of our experiment suggest that amitraz may reduce the heart rate by increasing acetylcholine through activating vagal nerves and ${\alpha}_2$-adrenoceptors could be involved in activating vagal nerves.

• 대한수의학회지
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• 제45권4호
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• pp.485-493
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• 2005

We studied the effects of trazodone on arterial blood pressure in anesthesized guinea pigs, and on vascular responses in isolated thoracic aorta. Trazodone produced a concentration-dependent relaxation in phenylephrine-precontracted endothelium intact (+E) rings, but not in a KCl-precontracted aortic rings. These relaxant effects of trazodone on +E rings were significantly greater than those on denuded (-E) rings. The trazodone-induced relaxation was suppressed by glibenclamide and tetrabutylammonium, but not by N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), methylene blue (MB), nifedipine, indomethacin, 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC) and clotrimazole. In vivo, infusion of trazodone elicited a significant decrease in arterial blood pressure. Trazodone-induced blood pressure lowering was markedly inhibited by intravenous pretreatment of prazosin but not by pretreatment of saponin, L-NNA, L-NAME, MB, nifedipine, glibenclamide, clotrimazole and NCDC. In addition, trazodone produced an increase in twitch force of isolated papillary muscle and left ventricular pressure of perfused heart. These findings suggest that the endothelium-independent vasorelaxant effect of trazodone may be explained by activation of $Ca^{2+}$-activated and ATP-sensitive $K^+$ channels, and the hypotensive effect of trazodone is not associated with cardiac contraction.

• 약학회지
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• 제45권1호
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• pp.78-84
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• 2001

Heme oxygenase is a rate-limiting enzyme in heme catabolism that cleaves heme to form biliverdin, iron, and carbon monoxide. Heme oxygenase-1 is expressed in many types of cells and tissues and is highly induced in response to oxidative stress. Carbon monoxide, one of the products of heme oxygenase, can stimulate soluble guanylate cyclase and dilate the vascular smooth muscle. So, the induction of heme oxygenase by lipopolysaccharide (LPS)-induced oxydative stress and the effect of the resultant carbon monoxide on aortic contractility were examined in this study. Zinc protoporphyrine IX (ZnPP), a inhibitor of heme oxygenase, elicited weak contraction of thoracic aortic ring, and this effect was more potent in aorta of LPS-treated rats than control and was blocked by methylene blue. The hyperreactivity to ZnPP in LPS-treated group was blocked by co-treatment with aminoguanidine. In the aortic ring of LPS-treated rats, ZnPP didn't change the vasoreactivity to phenylephrine or acetylcholine. ZnPP elicited hyper-tensive effect in concious rats, and pretreatment with LPS did not affect this effect. Prazosin significantly diminished the hypertensive effect of ZnPP. These results indicate that LPS induced heme oxygenase in aotra, and the resultant carbon monoxide diminished the aortic reactivity to vasoconstrictor.

• Archives of Pharmacal Research
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• 제11권1호
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• pp.65-73
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• 1988

The effects of clonidine on the negative chronotropic response induced by stimulation of vagus nerve were studied in the presence of propranolol in reserpinized and anesthetized rats. When the heart rate was decreased by stimulation of the vagus nerve, clonidine significantly inhibited vagally induced heart rate decrease (negative chronotropic response) in dose dependent manner. This inhibitory effect of clonidine was virtually abolished by phentolamine, ${\alpha}_1-\;and\;{\alpha}_2-adrenoceptor$ antagonist, and partially antagonized by prazosin, ${\alpha}_1-adrenoceptor$ antagonist. On the other hand, when the heart rate was decreased by the infusion of bethanechol, a muscarinic parasympathetic stimulant, clonidine had no effect on the bethanechol-induced heart rate decrease. These results suggest that clonidine inhibits vagally induced negative chronotropic response by activation of presynaptic ${\alpha}-adrenoceptors$ located on the parasympathetic cholinergic nerve terminal in the heart and this effect of clonidine is more related to ${\alpha}_2-adrenoceptors$ than ${\alpha}_1-adrenoceptors$.

• 약학회지
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• 제48권5호
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• pp.285-290
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• 2004

The purpose of this study is to prove how magnetic field (MF) acts on sympathetic neuro-transmissions using thermal response. Mice were divided into two groups and each one was exposed to MF (20 G, 24 hrs) or sham. Every vehicle or drugs were treated a half hour before the thermal response test. The pain threshold was lowered by MF (20 G, 24 hrs) alone. This reduction of pain threshold by MF was not blocked by a single treatment of $\alpha$-receptor antagonist (prazosin), $\alpha$$_2$-receptor agonist (clonidine, guanabenz), $\beta$$_1$-receptor antagonist (atenolol) or $\beta$$_1$,$\beta$$_2$-receptor antagonist (propranolol). But administration of $\alpha$$_2$-receptor antagonist (yohimbine) completely inhibited the decrease in pain threshold by MF. Moreover, it increased by high dose of yohimbine over normal condition. These results suggest that MF acts on sympathetic nerve terminal to induce hyperalgesia, in which pre-synaptic az receptor might be involved.