• 한국균학회지
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• 제22권4호
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• pp.325-331
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• 1994

좀구멍버섯균(Schizopora paradoxa)은 백색 부후 균으로 망간이 배지에 첨가되지 않으면 MNP와 GOX는 동시에 생성되지 않았으며 고농도의 망간 첨가시 (40ppm)에는 기본적 농도(11.15ppm)에 비해 MNP와 GOX가 모두 높은 활성을 보였다. 그러나 망간농도에 따른 균사생장량에는 별 차이가 없었다. 구리와 veratryl alcohol에 대해서도 같은 실험을 실시하였으나 농도에 따른 MNP와 GOX의 변화가 상관관계를 갖지 않는 것으로 나타났다. MNP와 GOX의 생성조절과 관련하여 cAMP의 영향을 조사한 결과 cAMP생성효소 억제제인 atropine을 농도별로 배양액에 첨가시 정도의 차이는 있었으나 MNP와 GOX생성이 동시에 억제되었다.

• The Korean Journal of Physiology
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• 제13권1_2호
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• pp.29-34
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• 1979

The present study was undertaken to investigate depressor action of tannic acid and the mechanism underlies it in the rabbit. The changes in arterial blood pressure were studied after intravenous administration of tannic acid in normal rabbits and the animals pretreated with atropine, propranolol, dibenamine, and hexamethonium. The results obtained were as follows; 1) Following administration of 1.5 mg/kg, 3.0 mg/kg, and 5.0 mg/kg of tannic acid into rabbits the maximum depressor responses observed were $12.0{\pm}0.9\;mmHg$, $23.4{\pm}1.0\;mmHg$, and $34.0{\pm}1.8\;mmHg$ respectively and generally depressor responses increased in proportion to dosage of tannic acid. 2) Since there were no changes in depressor responses to tannic acid in animals pretreated. separately with atropine, propranolol, dibenamine, and hexamethonium, the depressor responses appeared to be resulting from direct vasodilator action of tannic acid on the vascular smooth muscle. Comparing tannic acid and acorn extract in their mechanisms of depressor responses, it is strongly indicated that in acorn there might exist another depressor substance. 3) After administration of large doses of tannic acid, in addition to respiratory changes, the mean arterial blood pressure decreased markedly and was never recovered throughout the experiment. comma Therefore it is also suggested that the lethal action of tannic acid resides in a drastic decline of arterial blood pressure and in respiratory changes as well.

• The Korean Journal of Physiology and Pharmacology
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• 제7권3호
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• pp.169-174
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• 2003

${\gamma}$-Aminobutyric acid (GABA) has been reported to enhance exocrine secretion evoked not only by secretagogues but also by intrinsic neuronal excitation in the pancreas. The pancreas contains cholinergic neurons abundantly that exert a stimulatory role in exocrine secretion. This study was undertaken to examine effects of GABA on an action of cholinergic neurons in exocrine secretion of the pancreas. Intrinsic neurons were excited by electrical field stimulation (EFS; 15 V, 2 msec, 8 Hz, 45 min) in the isolated, perfused rat pancreas. Tetrodotoxin or atropine was used to block neuronal or cholinergic action. Acetylcholine was infused to mimic cholinergic excitation. GABA $(30{\mu}M)$ and muscimol $(10{\mu}M)$, given intra-arterially, did not change spontaneous secretion but enhanced cholecystokinin (CCK; 10 pM)-induced secretions of fluid and amylase. GABA (3, 10, $30{\mu}M$) further elevated EFS-evoked secretions of fluid and amylase dose-dependently. GABA (10, 30, $100{\mu}M$) also further increased acetylcholine $(5{\mu}M)$-induced secretions of fluid and amylase in a dose-dependent manner. Bicuculline $(10{\mu}M)$ effectively blocked the enhancing effects of GABA $(30{\mu}M)$ on the pancreatic secretions evoked by either EFS or CCK. Both atropine $(2{\mu}M)$ and tetrodotoxin $(1{\mu}M)$ markedly reduced the GABA $(10{\mu}M)$-enhanced EFS- or CCK-induced pancreatic secretions. The results indicate that GABA enhances intrinsic cholinergic neuronal action on exocrine secretion via the $GABA_A$ receptors in the rat pancreas.

• 한국임상수의학회지
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• 제26권5호
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• pp.476-479
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• 2009

Enucleation of a 9-year-old, spayed female Pekingese's right eye was scheduled because of recurrent eyeball rupture caused by chronic corneal ulcer and descemetocele. Scoliosis of the thoracic vertebra was observed on thoracic radiography. Complete blood count, electrolytes, serum chemistry profiles were within normal ranges except of alkaline phosphatase, which was markedly improved, compared with that of five months ago. Severe respiratory sinus arrhythmia was observed before induction of anesthesia, it disappeared after induction. Retrobulbar block was performed with 0.5% bupivacaine, 2% lidocaine, 0.1% epinephrine combination (4 : 1 : 0.2 ratio of volume) before start of surgery. After retrobulbar block, heart rate decreased from 110 to 76 beats/min and sinus arrhythmia recurred. It was considered as oculocardiac reflex caused by increase of intraorbital pressure from retrobulbar block, atropine (0.025 mg/kg, IV) was administered and intermittent positive pressure ventilation was started. Three minutes after atropine administration, abnormal waveform of the electrocardiograph was appeared, it suspected as ventricular or supraventricular tachycardia, so lidocaine (2 mg/kg, IV) was administered. Then, heart rate was maintained around 130 beats/min, and the surgery was finished without the other problems. Although, retrobulbar block is performed to provide analgesia and to prevent oculocardiac reflex in ophthalmic surgery, occasionally it could induce oculocardiac reflex by infiltrated volume.

• 대한한방내과학회지
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• 제27권2호
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• pp.471-479
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• 2006

Backgrounds & Objectives: Banhasasimtang granule(BHSST) has been used for the treatment of functional dyspepsia regarded as one of the gastric dysmotility disease. but its mechanisms of action are not well known yet: So we investigated the effects of BHSST on gastric emptying and its mechanisms of action in rats. Methods: Gastric emptying was measured by glass beads(1mm in diameter) expelled from the stomach for 60 min after administration of normal saline(NS) or BHSST 31mg/kg or 93mg/kg in rats. And by the same method gastric emptying was measured after administration of NS or BHSST 93mg/kg in rats treated with atropine sulfate(1mg/kg, s.c.), quinpirol HCI(0.3mg/kg, i.p.), NAME(NG-nitro-L-arginine methyl ester, 75mg/kg, s.c.) or cisplatin(10mg/kg, i.p.) to make delayed gastric emptying. Results: BHSST 93mg/kg improved gastric emptying more than NS or BHSST 31mg/kg(p=0.016). Under the delayed gastric emptying, BHSST 93mg/kg improved gastric emptying in the group treated with NAME$(5.00{\pm}3.101\;vs\;9.00{\pm}3.51,\;p\;=0.046)$, but aggravated it With atropine sulfate$(5.71{\pm}3.45\;vs\;2.57{\pm}1.62,\;p\;=0.050)$ and cisplatin$(12.7{\pm}2.29\;vs\;8.57{\pm}5.06,\;p\;=0.072)$. Conclusions: BHSST improves the gastric emptying through cholinergic and 5-hydroxytryptamine 3 receptors. Especially it is effective to improve gastric emptying delayed by NAME. So we expect that it would be effective in functional dyspepsia with impaired reservoir functions such as gastric adaptive relaxation.

• 대한한방내과학회지
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• 제28권2호
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• pp.242-249
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• 2007

Backgrounds & Objectives : Yukgunjatanggranule (YGJT) ha been used for the treatment of functional dyspepsia, regarded as one of the gastric dysmotility diseases, but its mechanisms of cation are not yet well known, We investigated the effects of YGJT on gastric emptying and its mechanisms of action in rats. Methods : Gastric emptying was measured by glass beads (1mm in diameter) expelled from the stomach for 1 hour and 2 hours after administration ofnormal saline (NS) or YGJT 41.6mg/kg or 124.8mg/kg in rats. By the same method, gastric emptying was measured only for 2 hours after administration of NS of YGJT 124.8mg/kg in rats treated with atropine sulfate (1mg/kg, s.c), quinpirole HCl(0.3mg/kg, i.p.), NAME (NG-nitro-L-arginine methyl ester, 75mg/kg, s.c.) or cisplatin (10mg/kg, i.p.) to delay gastric emptying. Results : YGJT 124.8mg/kg improved gastric emptying more than NS or YGJT 41.6mg/kg (p=0.046). Under delayed gastric emptying, YGJT 124.8mg/kg improved gastric emptying in the group treated with cisplatin ($3.1{\pm}1.3$ vs. $6.6{\pm}3.1$, p=0.015), quinpirole HCl ($4.7{\pm}2.8$ vs. $5.5{\pm}5.6$, p=0.874) and NAME ($2.2{\pm}1.4$ vs. $4.7{\pm}6.0$, p=0.414), but aggravated it with atropine sulfate ($1.8{\pm}0.9$vs. $1.7{\pm}1.0$, p=0.957). Conclusions : YGJT improves gastric emptying through the cholinergic pathwas, and shows some effect against the toxicity of cisplatin. Therefore, we expect that it would be effective in relieving gastrointestinal symptoms in functional dyspepsia patients and cisplatin-treated patients.

• 대한한방내과학회지
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• 제29권1호
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• pp.189-199
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• 2008

Background & Objective : Jichul-hwan(JCH) has been used for the treatment of functional dyspepsia, regarded as a gastric dysmotility disease. We investigated the effects of JCH on gastric motility and its mechanisms of action in rats. Methods : The gastric wall was injured by tracting a part of stomach body in rats. Gastric emptying was measured after administration of normal saline(NS) or JCH in normal rats and gastric wall injured rats. To evaluate the mechanism of JCH under delayed gastric emptying conditions, normal rats were treated with atropine sulfate(1mg/kg, s.c.), quinpirole HCl(0.3mg/kgg, i.p.), $NAME(N^{G}-nitro-L-arginine$ methyl ester, 75mg/kg s.c.) and cisplatin(10mg/kg, i.p.). The gastric slow waves were measured for 30 minutes before and after administration of each solution(NS, JCH). Results : JCH 110.1mg/kg improved gastric emptying for 2 hrs(p=0.014). JCH 110.1mg/kg improved gastric emptying in the gastric wall injured rats(p=0.001). Under the delayed gastric emptying, JCH 110.1mg/kg improved gastric emptying in the group treated with atropine $sulfate(1.83{\pm}0.96$ vs $8.43{\pm}8.46$, p=0.003), but aggravated it with quinpirole $HCl(4.7{\pm}2.9$ vs $1.61{\pm}2.09$, p=0.021). Administration JCH 110.1mg/kg increased EGG power in rats. Conclusions : JCH stimulates gastric motility through the cholinergic pathway, so we expect that it would be effective in the treatment of dysmotility-like functional dyspepsia with low activity of vagus nerve.

• 대한수의학회지
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• 제39권4호
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• pp.702-709
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• 1999

The present study was performed to elucidate the effects of extracellular $Ca^{2+}$ on contractile responses in isolated porcine coronary artery ring using by perivascular nerve stimulation (PNS). Especially, the study was focused on the source of $Ca^{2+}$ on $P_{2X}$-purinoceptor mediated muscle contraction which one of $P_2$-purinoceptor subtypes. The following results can be drawn from these studies : 1. The phasic contractions induced by PNS were inhibited with muscarinic receptor antagonist, atropine ($10^{-6}M$). 2. The phasic contractions induced by PNS were significantly inhibited by sequential treatment with atropine and adrenergic neural blocker, guanethidine ($10^{-6}M$). 3. The phasic contractions induced by PNS were inhibited with $P_{2X}$-purinoceptor desensitization by repetitive application of $\alpha$,$\beta$-Me ATP ($10^{-4}M$). 4. The phasic contractions induced by PNS were so weakened in calcium-free medium. 5. The phasic contractions induced by PNS were inhibited with calcium channel blocker, verapamil ($10^{-6}{\sim}5{\times}10^{-6}M$). 6. The phasic contractions induced by PNS on pretreated with verapamil ($10^{-6}{\sim}5{\times}10^{-6}M$) were not changed by $\alpha$,$\beta$-Me ATP ($10^{-4}M$). These results demonstrate that the neurogenic phasic contractions induced by PNS are due to adrenergic-, cholinergic- and $P_{2X}$-purinergic receptors and the origin of $Ca^{2+}$ on $P_{2X}$-purinoceptor mediated muscle contraction is extracellular $Ca^{2+}$ through plasmalemmal $Ca^{2+}$ channels.

• 대한수의학회지
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• 제27권1호
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• pp.19-25
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• 1987

To validate the comparision of proximal and distal large intestinal motility, the amplitude and frequency of spontaneous motility, the effect of acetylcholine, the effect of atropine on the response of acetylcholine, the effect of histamine and the effect of pyrilamine and cimetidine on the response of histamine were investigated in rabbit. The results were summarized as follows: 1. The amplitude of spontaneous motility was more powerful on the proximal large intestine than that of the distal large intestine, but the frequency of spontaneous motility was similar on the both proximal and distal large intestine in rabbit. 2. Acetylcholine caused the contraction of proximal and distal large intestine, and the contractile response were increased between the concentration of acetylcholne $10^{-9}$ and $5{\times}10^{-6}M$ and $10^{-7}$ and $10^{-4}M$ on the proximal and distal large intestine, respectively, with dose-dependent manner in rabbit. 3. The contractile response induced by acetylcholine was completely blocked by the post-treatment with cholinergic receptor blocker, atropine $10^{-6}M$. 4. Histamine caused the contraction of proximal and distal large intestine and the contractile response were increased between the concentration of histamine $10^{-9}$ and $5{\times}10^{-5}M$ and $10^{-5}$ and $10^{-3}M$ on the proximal and distal large intestine, respectively, with dose-depend ent manner in rabbit. 5. The contractile response induced by histamine was completely blocked by the pretreatment with $H_1$-receptor blocker, pyrilamine $10^{-6}M$, but not blocked by the pretreatment with $H_2$-receptor blocker, cimetidine $10^{-6}M$.

• The Korean Journal of Physiology and Pharmacology
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• 제2권4호
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• pp.443-454
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• 1998

The present study was attempted to investigate the effect of vasoactive intestinal polypeptide (VIP) on secretion of catecholamines (CA) and to establish whether there is the existence of a noncholinergic mechanism in adrenomedullary CA secretion from the isolated perfused rat adrenal gland. The perfusion into an adrenal vein of VIP $(3{\times}10^{-6}\;M)$ for 5 min or the injection of acetylcholine (ACh, $5.32{\times}10^{-3}\;M$) resulted in great increases in CA secretion. Tachyphylaxis to releasing effect of CA evoked by VIP was not observed by the repeated perfusion. The net increase in adrenal CA secretion evoked by VIP still remained unaffected in the presence of atropine or chlorisondamine. However, the CA release in response to ACh was greatly inhibited by the pretreatment with atropine or chlorisondamine. The releasing effects of CA evoked by either VIP or ACh were depressed by pretreatment with nicardipine, TMB-8, and the perfusion of $Ca^{2+}$-free medium. Moreover, VIP- as well as ACh-evoked CA secretory responses were markedly inhibited under the presence of $(Lys^1,\;Pro^{2.5},\;Arg^{3.4},\;Tyr^6)-VIP$ or naloxone. CA secretory responses induced by ACh and high $K^+\;(5.6{\times}10^{-2}\;M)$ were potentiated by infusion of VIP $(3{\times}10^{-6}M\;for\;5\;min)$. Taken together, these experimental results indicate that VIP causes CA release in a fashion of calcium ion -dependence, suggesting strongly that there exists a noncholinergic mechanism that may be involved in the regulation of adrenomedullary CA secretion through VIP receptors in the rat adrenal gland, and that VIP may be the noncholinergic excitatory secretagogue present in the chromaffin cells.