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Jeoung Hee Ha 15 Articles
The Effects of Ethanol on Cholinesterase Inactivation by Organophosphorous.
Hyoung Chul Choi, Jong Ho Kim, Jeoung Hee Ha, Kwang Yoon Lee, Won Joon Kim, Hyun Jae Woo, Chang Uk Huh, Soo Min Son, Eun Jin Chun
Yeungnam Univ J Med. 1999;16(2):326-332.   Published online December 31, 1999
DOI: https://doi.org/10.12701/yujm.1999.16.2.326
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BACKGROUND
In korea the agricultural community widely uses organophosphorous, and organophosphorous poisonings are increasing every year. We compared change in activity of acetylcholinesterase and pseudocholinesterase by organophosphorous and by the interaction of ethanol and organophosphorous. We also compared the effect of reversible anticholinesterase drugs, physostigmine and neostigmine. The object of this study is to investigate the effects of several anticholinesterase drugs and on how ethanol influences the activity of cholinesterase. MATERIALS AND METHODS: Fifteen male university students were randomly selected, and blood samples were taken from the antecubital vein. The acetylcholinesterase in the RBC and the pseudocholinesterase in the serum were extracted and separated. The enzyme activity change was measured by the electrometric method. After adding acetylcholine, the pH change was measured with a pH meter. RESULTS AND CONCLUSION: Our results indicated that reversible anticholinesterase drugs decreased the cholinesterase activity more efficiently than organophosphorous. The acetyl cholinesterase and pseudocholinosterase activity were decreased by ethanol. When ethanol was added, oxime a cholinesterase activator, increased acetylcholinesterase activity but dose not increased pseudocholinesterase activity.
The Effects of Anticholinesterase Drugs on Gastric Motility.
Hyoung Chul Choi, Jong Ho Kim, Jeoung Hee Ha, Kwang Yoon Lee, Won Joon Kim, Dong Suk Kwak, Sung Hee Kim, Phil Hyun Song, Ji Hyun Yeo
Yeungnam Univ J Med. 1999;16(2):318-325.   Published online December 31, 1999
DOI: https://doi.org/10.12701/yujm.1999.16.2.318
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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 ethanal on anticholinesterase drug-induced motility change. MATERIALS AND METHODS: After excision of stomach, 2x10mm circular musele 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, and irreversible anticholinesterase drug, increased ACh induced contraction of gastric smooth muscle strips and PAM, a cholinesterase activator, antagnized 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 ethanal.
Brain Benzodiazepine-like Molecules and Stress-anxiety Response.
Jeoung Hee Ha
Yeungnam Univ J Med. 1999;16(1):25-33.   Published online June 30, 1999
DOI: https://doi.org/10.12701/yujm.1999.16.1.25
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Benzodiazepines(BZDs) are among the widely prescribed drugs in the world. They are potent anxiolytic, antiepileptic, hypnotic, and muscle relaxing agents. There is an emerging model of the role of several neural systems in anxiety and their relation to the mechanism of action of BZDs. It has been postulated that BZD drugs exert their anxiolytic action by regulating GABAergic transmission in limbic areas such as the amygdala, in the posterior hypothalamus, and in the raphe nuclei. The involvement of the amygdala in the behaviors triggered by fear and stress has been suggested by many previous studies. In this review, reports about regulatory effects of endogenous BZD receptor ligands on the perception of anxiety and memory consolidation were summerized. These findings further support the contention that BZD receptor ligands modulate memory consolidation of averse learning tasks by influencing the level of stress and/or anxiety that accompanies a learning experience. The findings suggest that the decrease in the limbic levels of BZD-like molecules seen after the various behavioral procedures represent a general response to stress and/or anxiety, since it occurs in proportion to the level of stress and/or anxiety that accompany these tasks. In addition, these findings further support the hypothesis that the GABAA/BZD receptor complex in limbic structures plays a pivotal role in the stress and anxiety.
Effect of NG-nitro-L-arginine methyl ester and Methylene Blue on the Endotoxin-induced Vascular Hyporesponsiveness.
Hyoung Chul Choi, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim, Uy Dong Sohn
Yeungnam Univ J Med. 1997;14(2):337-349.   Published online December 31, 1997
DOI: https://doi.org/10.12701/yujm.1997.14.2.337
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The study was undertaken to examine the intensity of involvement of inducible nitric oxide synthase(iNOS) and cyclic GMP signal transduction pathway as one of the mechanisms of vaso-relaxative action of bacterial lipopolysaccharide (LPS) on the canine femoral artery strips. Canine femoral arteries were isolated and spiral strips of 10 mm long and 2 mm wide were made in the Tyroad solution of 0-4degrees C. The strips were prepared for isometric myography in Biancani's isolated muscle chamber contaning 1 ml of Tyrode solution, which was maintained with pH 7.4 by areation with 95% O2/5% CO2 at 37degrees C and nitric oxide (NO) production was measured simulltaneously with isolated nitric oxide mrter. LPS induced NO production, suppressed the phenylephrine (PE) induced contraction and enhanced the acetylcholine (ACh) induced relaxation. NG-nitro-L-arginine methyl ester (L-NAME), an NOS inhibitor, methylene blue, a guanylyl cyclase inhibitor, potentiated PE induced contraction and suppressed ACh induced relaxation on the LPS treated strips. The inhibitory potency of methylene blue for LPS induced vascular hyporeponsiveness was stronger than that of L-NAME. These result suggest that in canine femoral artery, both iNOS and cyclic GMP signal transduction pathway are related with LPS indused vascular hyporeponsiveness, but in minor with iNOS and in major with cyclic GMP signal transduction pathway.
Effect of Baclofen on the Cholinergic Nerve Stimulation in Isolated Rat Detrusor
Kwang Youn Lee, Keun Mi Lee, Eun Mee Choi, Hyoung Chul Choi, Jeoung Hee Ha, Won Joon Kim
Yeungnam Univ J Med. 1995;12(2):246-259.   Published online December 31, 1995
DOI: https://doi.org/10.12701/yujm.1995.12.2.246
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This study aimed to investigate the mechanism of action of baclofen on the detrusor muscle isolated from rat. Rats (Sprague-Dawley) were sacrificed by decapitation and exsanguination. Horizontal muscle strips of 2 mm × 15 mm were prepared for isometric myography in isolated muscle chamber bubbled with 95% / 5%-OZ / CO2 at 371C, and the pH was maintained at 7.4. Detrusor strips contracted responding to the electrical field stimulation (EFS) by 2 Hz, 20 msec, monophasic square wave of 60 VDC. The initial peak of EFS-Induced contraction was tended to be suppresed by α,β-methylene-adenosine 5'-triphosphate (mATP), a partial agonist of purinergic receptor, and baclofen, a GABAB receptor agonist (statistically nonsignificant). The late sustained contraction by EFS was suppressed significantly (p<0.05) by additions of atropine, a cholinergic muscarinic receptor antagonist and baclofen. The adenosine 5'-triphosphate-induced contraction was completely abolished by mA TP but not by baclofen. In the presence of atropine, the subsequent addition of acetylcholine could not contract the muscle strips: but the addition of acetylcholine in the presence of baclofen evoked a contraction to a remarkable extent. These results suggest that in the condition of present study, the cholinergic innervation may play a more important role than the purinergic one, and baclofen suppresses the contractility of rat detrusor by the stimulation of the GABA receptors to inhibit the release of neurotransmitter from the cholinergic nerve ending
Endogenous benzodiazepine receptor ligands
Jeoung Hee Ha
Yeungnam Univ J Med. 1995;12(1):158-159.   Published online June 30, 1995
DOI: https://doi.org/10.12701/yujm.1995.12.1.158
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Characteristics of Potassium Channel in the Isolated Rat Detrusor Muscle.
Myeong Soo Jang, Eun Mee Choi, Jeoung Hee Ha, Kang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1994;11(2):363-374.   Published online December 31, 1994
DOI: https://doi.org/10.12701/yujm.1994.11.2.363
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The purpose of this study was to investigate the characteristics or the potassium channels existing in the rat urinary bladders. Smooth muscle strips of rat detrusor urinae were examined by isometric myography. Relaxation responses of detrusor muscle strips to the three potassium channel openers pinacidil, a cyanoguanidine derivative, BRL 38227, a benzopyran derivative and RP 52891, a tertrahydrothiopyran derivative were examined. The potassium channel openers reduced the basal tone, and the rank order of potency was RP 52891>pincidil>BRL 38227. Procaine, an inhibitor of the voltage-sensitive potassium channel tended to increase the basal tone, but it did not affect the relaxant effects of the calcium-activated potassium channel opener did not antagonize the relaxant effects, but it reduced the Emax of RP 52891 and BRL 38227. Glibenclamide, an inhibitor of the ATP-sensitive potassium channel, antagonized the relaxant effects of pinacidil, RP 52891 and BRL 38227 reducing the Emax of RP 52891 and BRl 38227. Galanin which inhibits secretion of insulin through opening the ATP-sensitive potassium channels in pancreatic β-cells rather increased the basal tone of the isolated detrusor strips. These results suggest that the urinary bladder of the rat has mainly the ATP-sensitive, glibenclamide sensitive potassium channel, which is a different type from that in the pancreatic β-islet cells.
Effects of octreotide on the contractility of isolated rat vas deferens.
Sun Ae Jang, Oh Cheol Kwon, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1993;10(1):144-156.   Published online June 30, 1993
DOI: https://doi.org/10.12701/yujm.1993.10.1.144
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This study was performed to investigate the effect of octreotide on the contractility of rat vas deferens. The -smooth muscle strips isolated from the prostatic portion were myographied in isolated organ bath. Electric -field stimulation (monophasic square wave, duration : 1. mSec, voltage : 50 V, frequency : 5 Hz or 30 Hz, train : 10 Sec) produced reproducible contraction. The contraction was composed of two component, first phasic component (FPC) and second tonicc component (STC).. These contractions were abolished by -tetrodotoxin (1 microM). Octreotide inhibited the field stimulation induced contractions both FPC and STC concentration- dependently. The FPC was decreased by a desentization of purinergic receptor by pretreatment of mATP, and the STC was decreased by pr,,creatment of reserpine (3 mg/kg, EP) 24 hours before experiments. Octreotide reduced the field stimulation induced contraction in the presence of mATP and of reserpinized muscle strips. The inhibitory effect of octreotide was more potent at 5 Hz than at 30 Hz. Octreotide did not affect basal ton and exogenous norepinephrine- or ATP-induced contraction. These results suggest that octreotide inhibit the contractility of the isolated rat vas deferens by inhibition of the release of neurotransmitters, both ATP and norepinephrine from adrenergic nerve terminal.
Inhibitory of γ-aminobutyric acid on the contractility of isolated rat vas deferens.
Ki Young Ahn, Oh Cheol Kwon, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1992;9(2):382-395.   Published online December 31, 1992
DOI: https://doi.org/10.12701/yujm.1992.9.2.382
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GABA is an inhibitory neurotransmitter in central nervous system and produce sedative, antianxiety and muscle relaxing effects via GABA(A) receptor or GABA(B) receptor. Recently it is known that GABA is widely distributed throughout peripheral organs and may play a physiological role in certain organ. The vas deferens is innervated by species-difference. These study, therefore, was performed to investigate the mode and the mechanism of action of GABA on the norepinephrine-, ATP- and electric stimulation-induced contraction of vas deferens of rat. Sprague-Dawley rats were sacrificed by cervical dislocation. The smooth muscle strips were isolated from the prostatic portion and were mounted in the isolated muscle bath. PSS in the bath was aerated with 95/5%-O₂/CO₂ at 33℃. Muscle tensions were measured by isometric tension transducer and were recorded by biological recording system. 1. GABA, muscimol, a GABA(A) agonist, and baclofen, a GABA(B) agonist inhibited the electric field stimulation (EFS, 0.2Hz, 1mSec, 80V, monophasic square wave)-induced contraction with a rank order of potency of GABA greater than baclofen greater than muscimol. 2. The inhibitory effect of GABA was antagonized by delta aminovaleric acid (DAVA), a GABA(B) antagonist, but not by bicuculline, a GABA(A) intagonist. 3. The inhibitory effect of baclofen was antagonized by DAVA, but the effect of muscimol was not antagonized by bicuculline. 4. Exogenous norepinephrine (NE) and ATP contracted muscle strip concentration dependently, but the effect of acetylcholine was negligible and GABA did not affect the NE-and ATP-induced contractions. 5. GABA, baclofen and muscimol did not affect basal tone, and GABA did not affect the NE-and ATP-induced contractions. 6. EFS-induced contraction was inclucling 2 distinctable components. The first phasic component was inhibited by beta gamma-methylene ATP (mATP), a desensitizing agent of APT receptor and the second tonic component was reduced by pretreatment of reserpine (3 mg/Kg, IP). 7. GABA inhibited the EFS-induced contraction of reserpinized strips, but not the mATP-treated strips. These results suggest that in the prostatic portion of the rat vas deferens, adrenergic and purinergic neurotransmissions are exist, and GABA inhibits the release of ATP via presynaptic GABA(B) receptor on the excitatory neurons.
Effect of diazepam on the oxytocin induced contraction of the isolated rat uterus.
Yoon Kee Park, Sung Ho Lee, Oh Cheol Kwon, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1992;9(2):359-381.   Published online December 31, 1992
DOI: https://doi.org/10.12701/yujm.1992.9.2.359
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This study was designed to investigate the effect of diazepam on the spontaneous contraction and oxytocin induced contraction of the isolated rat uterus. Female rat (Sprague-Dawley) pretreated with oophorectomy and 4 days administration of estrogen. Weighing about 200 g, was sacrificed by cervical dislocation, and the uteruses were isolated. A longitudinal muscle strip was placed in temperature controlled (37℃) muscle chamber containing Locke's solution and myographied isometrically. Diazepam inhibited the spontaneous contraction and oxytocin induced contraction of the isolated rat uterus in a concentration-dependent manner. GABA, muscimol, a GABA A receptor agonist, bicuculline, a competitive GABA A receptor antagonist, picrotoxin, a non competitive GABA A receptor antagonist, baclofen, a GABA B receptor agonist, and delta-aminovaleric acid, a GABA B receptor antagonist, did not affect on the spontaneous and oxytocin induced contraction of the isolated rat uterus. The inhibitory actions of diazepam on the spontaneous and oxytocin induced contraction were not affected by all the GABA receptor agonists and antagonists, but exceptionally potentiated by bicuculline. This potentiation-effect by bicuculline was not antagonized by muscumol. In normal calcium PSS, addition of calcium restored the spontaneous contraction preinhibited by diazepam and recovered the contractile of oxtrocin preinhibited by diazepam. A23187, a calcium inophore, enhanced the restoration of both the spontaneous and oxytocin induced contraction by addition of calcium. In calcium-free PSS, diazepam suppressed the restoration of spontaneous motility by addition of calcium but allowed the recovery of spontaneous motility to a considerable extent. Diazepam could not inhibit some development of contractility by oxytocin in calcium-free PSS, but inhibited the increase in contractility by subsequent addition of calcium. These results suggest that the inhibitory action of diazepam on the rat uterine motility does not depend on or related to GABA receptors and that diazepam inhibits the extracellular calcium influx to suppress the spontaneous and oxytocin induced contractilities.
Existance of cholinergic and purinergic receptor on the detrusor muscle of rat urinary bladder.
Tae Su Choi, Oh Cheol Kwon, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1991;8(2):138-149.   Published online December 31, 1991
DOI: https://doi.org/10.12701/yujm.1991.8.2.138
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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℃ and aerated with 95% O²/5% Co². Isometric myography was performed, 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 incubating of the strips in the presence of high concentration 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.
Effect of GABA on the contratility of small intestine isolated from rat.
Joon Young Huh, Oh Cheol Kwon, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1991;8(2):95-105.   Published online December 31, 1991
DOI: https://doi.org/10.12701/yujm.1991.8.2.95
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This study was designed to investigate the effect of GABA and related substances on the spontaneous contraction of rat small intestine. The rats (Sprague-Dawley), weighing 200-250g, were sacrificed by cervical dislocation, and the small intestine was isolated. Longitudinal muscle strips from duodenum, jejunum and ileum were suspended in Biancani's isolated muscle chambers and myographied isometrically. GABA and muscimol, a GABA A receptor agonist relaxed the duodenum and jejunum significantly, but baclofen-induced relaxation in those muscle strips negligible. The effectiveness of GABA and muscimol in various regions were the greatest on duodenum, and greater on jejunum than on ileum The effect of GABA and muscimol was antagonized by bicuculline, a competitive GABA A receptor antagonist and picrotoxin, a noncompetitive GABA A receptor antagonist. Duodenal relaxation induced by GABA and muscimol was unaffected by hexamethonium, but was prevented by tetrodotoxin. These results suggest that GABA inhibit the contractility of smooth muscle with distinct regional difference of efficacy, and the site of inhibitory action is the GABA A receptor existing at the presynaptic membrane of postganglionic excitatory nerves.
The Effects of Diazepam on the Carbachol Induced Contraction of the Isolated Rat Ileum.
Jung Ok Kim, Oh Cheol Kwon, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1989;6(2):13-22.   Published online December 31, 1989
DOI: https://doi.org/10.12701/yujm.1989.6.2.13
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To investigate the effect of diazepam on the contractility of the intestinal smooth muscle, longitudinal muscle strip isolated from rat ileum was prepared for myography in isolated organ bath. 1) Basal tone of ileal muscle was reduced by diazepam concentration-dependently. 2) Higher concentrations (30 and 100 microM) of diazepam inhibited (p<0.05, p<0.001) The carbachol-induced contraction in a concentration-dependent manner; but lower concentration of diazepam (10 microM) enhanced (p<0.05). 3) Histamine-induced contraction was inhibited by pretreatment with diazepam in a concentration-dependent manner. 4) Ca⁺⁺-induced tension recovery in calcium-free solution was inhibited in the presence of diazepam concentration-dependently. These results suggest diazepam reduces the contractility of the longitudinal muscle isolated from rat ileum via interference with influx of calcium into the muscle cells.
Effect of Carbamazepine on the Ouabain-Induced Arrhythmia in Rabbits.
Eui Hong Kim, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1986;3(1):279-285.   Published online December 31, 1986
DOI: https://doi.org/10.12701/yujm.1986.3.1.279
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Carbamazepine is a derivative of iminostilbene with carbamoyl group and related chemically to the tricyclic antidepressants. Carbamazepine has been introduced for treatment of trigeminal neuralgia. Recently it is used as an antiepileptic agent such as diphenylhydantoin. Antiepileptic drugs are known to affect experimentally induced cardiac arrhythmia and are now widely used clinically for treatment of ventricular tachyarrhythmias, particularly those produced by digitalis intoxication. Steiner et al. (1970) reported that carbamazepine was found to be very effective in converting ventricular tachycardia due to digitalis toxicity to normal sinus rhythm. Clinically bradycardia, complete heart block, ventricular standstill and Adams-stokes attack were reported in the course of carbamazepine treatment. The purpose of this study was to investigate the effects of carbamazepine on the ouabain-induced arrhythmia in vivo. The rabbits of either sex, weighing from 1.6 to 3.2 kg were anesthetized by urethane. After the trachea was cannulated, the rabbits were ventilated with room air using a respirator. Drugs were given into polyethylene cannula in the femoral vein. Blood pressure were recorded by physiograph via pressure tranducer connected with the cannula in the femoral artery. EKG were recorded by physiograph via electrode implanted in both fore leg and left hind leg. The results are summarized as follows 1. Arrhythmia was induced by continuous infusion of ouabain (65±8.8 µg/kg). 2. Single administration of ouabain (64 µg/kg) induced arrhythmia which was persisted for 7-8 min. 3. Ouabain induced arrhythmia was restored to normal sinus rhythm by administration of carbamazepine (the more dosage, the less frequent and the longer duration). 4. Severe bradycardia, A-V block, atrial fibrillation were seen on the EKG after injection of carbamzepine alone. By the above results, it may be concluded that carbamzepine inhibits the ouabain-induced arrhythmia by dose-dependent.
Effect of Corticosteroids on Renal Excretion of Lithium.
Shin Yul Oh, Jeoung Hee Ha, Kwang Youn Lee, Won Joon Kim
Yeungnam Univ J Med. 1986;3(1):229-235.   Published online December 31, 1986
DOI: https://doi.org/10.12701/yujm.1986.3.1.229
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Lithium salts are being used increasingly to treat patient with affective disorders, especially acute mania, or bipolar manic-depressive illness. For therapeutic effect the lithium content must be maintained at or above a particular level. Lithium poisoning due to overdosage may be seen occasionally, and its course is determined primarily by the rate of renal lithium elimination. A search is therefore indicated for procedures that could raise the lithium clearance. In a number of reports renal lithium excretion has been studied in relation to the excretion of water, sodium, potassium and hydrogen, but effects of sodium or water on the lithium excretion has not yet been clarified. Hence the present study was undertaken to investigate the effects of corticosteroid on the excretion of lithium ion. The female rat (Sprague-Dowley), weighing from 200 to 300g, was injected with 50mg/kg of lithium chloride intraperitoneally, and then injected with graded dosage of fludrocortisones and dexamethasone in each group. During the injected rats were incubated in metabolic cage, 24 hour urine of rats were collected. At 24 hours after injection, the rats were sacrificed with guillotine, the blood were collected. And then the concentrations of Na⁺, K⁺, Li⁺ of collected urine and serum were checked by Flame photometer. The results are summarized as follows 1. Fludrocortisone decreased the serum concentration of lithium and increased the urinary excretion of lithium. 2. In the group treated with low dose of dexamethasone (0.1 mg/kg), the serum concentration of lithium was decreased and high dose of dexamethasone (1 mg/kg) increased the urinary excretion of lithium. 3. Fludrocortisone increased the urinary [Na⁺]/[K⁺] in serum and decreased [Na⁺]/[K⁺] inurine, but opposite effects were occurred in dexamethasone. By above results, it may be concluded that corticosteroid increased the urinary excretion of lithium and decreased the serum concentration of lithium, but it seems to be there in no relationship between these effects of corticosteroid and of the renal Na⁺ or K⁺ transport.

JYMS : Journal of Yeungnam Medical Science