• Journal of Pharmaceutical Investigation
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• v.9 no.2
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• pp.22-30
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• 1979

Effects of Akebiae Lignum, whose scientific name is Akebia quinata Decaisne, on the blood pressure were investigated with EtOH extract in whole and spinal rabbits. Akebia Lignum EtOH extract (AEE), when given intravenously, produced a fall in blood pressure not only in whole rabbit but also in spinal rabbit and AEE administered into a lateral cerebral ventricle of whole rabbit did not elicit a fall in blood pressure. The depressor responses of the whole rabbit to intravenous AEE were weakened by treatment of the animals with atropine and chlorisondamine but not by vagotominijation, phentolamine avil, and then the depressor action causing by AEE in the whole rabbit was not affected by pretreatment of physostigmine which is cholinesterase inhibitor and of hemicholinium which blocks acetylcholine synthesis by interfering with choline uptake in nerves. These observations suggest that the hypotensive action of AEE of which component is not affected by cholinesterase is due to direct action at parasympathetic receptor.

• Journal of The Korean Society of Clinical Toxicology
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• v.7 no.1
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• pp.23-25
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• 2009

A 21-year-old woman ingested 1,250 mg of diphenhydramine in a single overdose. Diphenhydramine, a rare ingredient in over-the-counter medication, is used to treat insomnia in Korea. Toxicity is usually limited to anticholinergic symptoms. The standard approach to therapy for the treatment of diphenhydramine overdose is supportive care, including physostigmines and sodium bicarbonates. Here, we review the literature and for the first time report a case of acute diphenhydramine overdosage in Korea, complicated with seizures.

• Archives of Pharmacal Research
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• v.19 no.6
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• pp.520-528
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• 1996

The involvement of the cyclic AMP (cAMP) effector system in the release of endogenous dopamine and acetylcholine from the rat neostriatum was assessed. Forskolin, an activator of adenylate cyclase, was used to enhance cAMP production, and the consequence of this enhancement on the spontaneous and potassium stimulated release of dopamine and acetylcholine was evaluated. Neostriatal slices were prepared from Fischer 344 rats and after a preincubation period the release of each endogenous neurotransmitter was measured from the same slice preparation. To measure acetylcholine release the slice acetylcholinesterase (AChE) activity was inhibited with physostigmine, but the release from slices with intact AChE activity was also determined (choline, instead of acetylcholine was detected in the medium). Under both conditions forskolin induced a significant dose-dependent increase in the potassium-evoked release of dopamine. In the same tissue preparations the release of neither acetylcholine (AChE inhibited) nor choline (AChE intact) was affected by forskolin. The results indicate that the CAMP second messenger system might be involved in neuronal mechanisms that enhance neostriatal dopamine release, but stimulation of this second messenger by forskolin does not further enhance neostriatal acetylcholine release.

• Proceedings of the Ginseng society Conference
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• 1993.09a
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• pp.164-170
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• 1993

Panax ginseng has been reported to protect animals or to help them recover from physical, chemical, or biological stress. The antistress effects of ginseng were evaluated through the measurement of adrenal ascorbic acid, rectal temperature, and plasma level of glucose. lipids and corticosterone. During the treadmill experiments of the antifatigue study, the groups of rats receiving P. ginseng or P. quinquefolius extracts were consistently found to leave fewer fecal boli on the wheel compared with controls. This phenomenon may be due to the reported antistress effects of ginseng. Another possibility could be that the Panax species examined produced anticholinergic effects which in turn inhibited the production of fecal boli. After an anticholinergic study. employing physostigmine and atropine as controls, anticholinergic effect was found not essential for the decrease of fecal boli number left on the wheels during antifatigue studies. The results were consistent with the antistress activity reported previously. Even though the active constituents responsible for the antistress effects of ginseng remained to be determined, the fecal boli counts for stressed rats can be employed as a new protocol for evaluating the antistress effects of ginseng.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.31-42
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• 1989

The effect of metoclopramide (MCP), which is well-known as a selective dopaminergic antagonist used in treating esophageal refulx, gastroparesis and emesis induced by anticancer chemotherapy, on secretion of catecholamines (CA) in the perfused isolated rat adrenal gland was investigated. MCP given into an adrenal vein produced the dose-related increase in CA secretion from the adrenal gland. The secretory effect of CA evoked by MCP was inhibited markedly by atropine-pretreatment. but only partially blocked when chlorisondamine was added. The secretion of CA induced by MCP was potentiated by pretreatment with physostigmine, adenosine or ouabain. However, MCP-induced CA secretion was suppressed significantly by perfusion of calcium-free Krebs solution containing 5 mM-EGTA for 30 min. Perfusion of MCP (200 ug/30 min.) attenuated the secretory effect of CA evoked by potassium chloride or acetylcholine. These experimental results demonstrate that metoclopramide releases CA significantly by a calcium-dependent exocy totic mechanism. It is thought that the secretory effect of metoclopramide is due to activation of cholinergic muscarinic receptors present in the adrenal gland rather than nicotinic receptors and partly to the direct action on the chromaffin cell itself.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.31-42
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• 1988

The effect of Panaxadiol(PD), which is an active component of Korean Ginseng Saponins, on the secretion of catecholamines (CA) from the rabbit adrenal gland and its mode of action were investigated in the present study. $PD(400{\mu}g)$ increased significantly the secretion of CA from the isolated perfused rabbit adrenal gland. PD-induced secretion of CA was reduced markedly by treatment of atropine, CA secretion induced by Ach or PD was potentiated significantly by physostigmine-treatment. Chlorisondamine did inhibit CA secretion of PD or Ach. Perfusion of $PD(400{\mu}g)$ for 30 min enhanced the secretory activity of CA by Ach. Ouabain weakened the secretory response induced by PD but rather enhanced the response by Ach. Adenosine-treatment resulted in marked enhancement of CA secretion by PD or Ach, Pefusion with $Ca^{2+}-free$ Krebs containing EGTA (5 mM) for about 30 min totally blocked secretory effect induced by Ach and also weakened that by PD. From the above experimental results, it is suggested that PD causes secretion of catecholamines from the rabbit adrenal gland by a calcium-dependent exocytotic mechanism. The secretory effect of PD is due to the stimulation of cholinergic muscarinic and nicotinic receptors present in the adrenal gland and partly to a direct action on the chromaffin cell itself.

• Journal of Yeungnam Medical Science
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• v.16 no.2
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• pp.318-325
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• 1999

Background: Anticholinesterase drug inhibits acetylcholinesterase(AChE), induce accumulation of acetylcholine(ACh) near cholinergic receptors and cholinergic stimulation. This experiment was performed to study the effects of anticholinesterase drugs on gastric motility and the effect of ethanol on anticholinesterase drug-induced motility change. Materials and Methods: After excision of stomach, $2{\times}10mm$ circular muscle strips were made, which were then fixed to the isolated muscle chamber. An isometric tension transducer was used to measure the contraction change of the gastric smooth muscle strips after drug addition. Results: Fenthion, an irreversible anticholinesterase drug, increased ACh induced contraction of gastric smooth muscle strips and PAM, a cholinesterase activator, antagonized this action. Physostigmine, a reversible anticholinesterase drug, also increased the ACh induced contraction. The gastric motility was decreased by PAM. Ethanol, which is known to induce smooth muscle relaxation, inhibited the increase of contraction by fenthion. Conclusion: These results indicate that irreversible and reversible anticholinesterase drugs increase gastric motility and antagonized by cholinesterase activating drugs. And when exposed to both ethanol and anticholinesterase drug, gastric motility was decreased by the smooth muscle relaxation effect by ethanol.

• Journal of Yeungnam Medical Science
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• v.8 no.2
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• pp.138-149
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• 1991

This study was aimed at investigation of the stimulatory innervations on the rat urinary bladder. Detrusor muscle strips of 15 mm long were suspended in isolated muscle chambers containing 1 ml of PSS maintained at $37^{\circ}C$ and aerated with 95% $O_2/5%CO_2$. Isometric myography was perfomed, and the results were as followings : Muscle strips showed "on-contraction" by electric field stimulation (EFS) frequency-dependently. The EFS-induced contraction was not affected by hexamethonium, a ganglion blocker, but abolished, by tetrodotoxin, a nerve conduction blocker. Physostigmine, a cholinesterase inhibitor enhanced the EFS-induced contraction which was inhibited by hemicholinium, an inhibitor of choline uptake at the cholinergic nerve ending. Such an EFS-induced contraction was antagonized by atropine only partially, and the atropine-resistant portion was completely abolished by the desensitization of purinergic receptors by prolonged incubatin of the strips in the presence of high concentratin of ATP. Bethanechol, a cholinergic agonist, elicited concentration-dependent contraction. Adenosine triphosphate (ATP), a purinergic agonist, induced a weak but concentration-dependent contraction of short duration. Bethanechol-induced contraction was not affected by ATP-desensitization, and ATP-induced contraction was not affected by tetrodotoxin. These results suggest that there are at least two main stimulatory components of innervations in the detrusor muscle, cholinergic muscarinic and purinergic ; and those receptors are independent each other.

• The Korean Journal of Pharmacology
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• v.23 no.2
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• pp.77-85
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• 1987

This study was carried out to determine the role of cholinoceptors in the ventrolateral medulla on central control of blood pressure (BP) and heart rate (HR). In rats anesthetized with urethane and paralyzed, microinjections of the neuroexcitatory amino acid L-glutamate (300 ng/site) were performed to functionally identity the vasopressor area (VLPA) and the vasodepressor area (VLDA) in the ventrolateral medulla oblongata. 1. The bilateral microinjection of carbachol (300 ng/site) into the VLPA produced significantly an increase in BP and HR which was not blocked by bilateral pretreatment of hexamethoium ($4\;{\mu}g/site$). 2. The bilateral microinjection of physostigmine (200 ng/site) and oxotremorine (300 ng/site) into the VLPA produced significantly an increase in BP respectively. 3. The bilateral microinjection of atropine ($4\;{\mu}g/site$) into the VLPA produced significantly a decrease in BP and HR. 4. The bilateral micro injection of acetylcholine (500 ng/site) and dimethylphenylpiperazinium (500 ng/site) into the VLDA produced significantly a decrease in BP and HR respectively. 5. The depressor and bradycardiac responses elicited by the bilateral microinjection of acetylcholine (500 ng/site) into the VLDA were blocked by bilateral pretreatment of hexamethonium ($4\;{\mu}g/site$). The results suggest that the activation of cholinoceptors in VLPA produce hypertensive and tachycardiac responses which may be mediated by muscarinic receptors, and the activation of cholinoceptors in VLDA produce hypotensive and bradycardiac responses which may be mediated by nicotinic receptors.

• Proceedings of the Ginseng society Conference
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• 1988.08a
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• pp.55-62
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• 1988

The effect of panaxadiol (PD). an active component of Korean ginseng saponins on the secretion of catecholamines (CA) from the rabbit adrenal gland and its mode of action were investigated. PD ($400\;{\mu}g$) increased significantly the secretion of CA from the isolated perfused rabbit adrenal gland. PD-induced secretion of CA was reduced markedly by treatment with atropine. CA secretion induced by Ach or PD was potentiated by physostigmine treatment. Chlorisondamine inhibited CA secretion of PD or Ach. Perfusion of PD ($400\;{\mu}g$) for 30 minutes enhanced the secretory activity of CA by Ach. Ouabain weakened the secretory rsponse caused by PD but enhanced the response by Ach. Adenosine treatment resulted in marked increase in CA secretion by PD or Ach. Perfusion with calcium free Krebs solution containing 5 mM EDTA for 30 minutes completely blocked the secretory effect induced by Ach and also weakened that evoked by PD. It is suggested that PD causes the secretion of CA from the rabbit adrenal gland by a calcium dependent exocytotic process. The secretory effect of PD is due to the stimulation of cholinergic muscarinic and nicotinic-receptors present in the adrenal gland partly by direct action on the chromaffin cell.