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유병식,민순영,서유석,최철희,이은화,임동윤 대한약리학회 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.4
The purpose of the present study was to examine the effect of naltrexone, an opioid antagonist, on secretion of catecholamines (CA) evoked by cholinergic nicotinic stimulation and membrane-depolarization from the isolated perfused rat adrenal gland and to establish the mechanism of its action. Naltrexone (3×10-6 M) perfused into an adrenal vein for 60 min produced time-dependent inhibition in CA secretory responses evoked by ACh (5.32×10-3 M), high K+ (5.6×10-2 M), DMPP (10-4 M) and McN-A-343 (10-4 M). Naltrexone itself did also fail to affect basal CA output. In adrenal glands loaded with naltrexone (3×10-6 M), the CA secretory responses evoked by Bay-K-8644, an activator of L-type Ca2+ channels and cyclopiazonic acid, an inhibitor of cytoplasmic Ca2+-ATPase, were also inhibited. However, in the presence of met-enkephalin (5×10-6 M), a well-known opioid agonist, the CA secretory responses evoked by ACh, high K+, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Collectively, these experimental results demonstrate that naltrexone inhibits greatly CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that this inhibitory effect of naltrexone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of Ca2+ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.
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유병식,나덕미,강미영,임동윤 대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.6
The present study was attempted to investigate whether polyphenolic compounds isolated from wine, which is brewed from Rubus coreanum Miquel (PCRC), may affect the release of catecholamines (CA) from the isolated perfused adrenal medulla of the spontaneously hypertensive rats (SHRs), and to establish its mechanism of action. PCRC (20∼180μg/ml) perfused into an adrenal vein for 90 min relatively dose-dependently inhibited the CA secretory responses to ACh (5.32 mM), high K+ (56 mM), DMPP (100μM) and McN-A-343 (100μM). PCRC itself did not affect basal CA secretion (data not shown). Also, in the presence of PCRC (60μg/ml), the CA secretory responses to veratridine (a selective Na+ channel activator (10μM), Bay-K-8644 (a L-type dihydropyridine Ca2+ channel activator, 10μM), and cyclopiazonic acid (a cytoplasmic Ca2+-ATPase inhibitor, 10μM) were significantly reduced, respectively. In the simultaneous presence of PCRC (60μg/ml) and L-NAME (an inhibitor of NO synthase, 30μM), the inhibitory responses of PCRC on the CA secretion evoked by ACh, high K+, DMPP, and Bay-K-8644 were considerably recovered to the extent of the corresponding control secretion compared with that of PCRC-treatment alone. The level of NO released from adrenal medulla after the treatment of PCRC (60μg/ml) was greatly elevated compared with the corresponding basal level. Taken together, these results demonstrate that PCRC inhibits the CA secretion from the isolated perfused adrenal medulla of the SHRs evoked by stimulation of cholinergic receptors as well as by direct membrane-depolarization. It seems that this inhibitory effect of PCRC is mediated by blocking the influx of calcium and sodium into the adrenal medullary chromaffin cells of the SHRs as well as by inhibition of Ca2+ release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of NO synthase.
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기관내 삽관시 Lidocaine 투여방법에 의한 심혈관계 반응의 비교
유병식 대한마취과학회 1991 Korean Journal of Anesthesiology Vol.24 No.4
The purpose of this study was to compare the cardiovascular changes with various administration method of lidocaine. This study was performed 40 patients scheduled for elective surgery at chosun university hospital. Patients were randomly assigned to recieve lidocaine by intravenous, larynogotracheal spray, transtracheal injection before tracheal intubation. Systolic blood pressure(SBP), diastolic blood pressure(DBP) mean arterial pressure(MAP) and Heart rate(HR) were measured at preinduction and 1, 2, 3, & 5 minutes after intubation. The results were as follows; 1) Control group; not administered lidocaine; SBP, DBP, MAP % HR were significantly increased at 1, 2 minutes after intubation(P$lt;0.05, P$lt;0.01). 2) Group 1; intravenous lidocaine administration(2 mg/kg); SBP, DBP, MAP were increased but not statistically significant. Heart rate was significantly increased at 1, 2, 3 minutes after intubation(P$lt;0.05, P$lt;0.01). Compared with control group, SBP, DBP & MAP were statistically significant (P$lt;0.05). 3) Group 2; laryngotracheal spray(2 mg/kg); Similar to group 1 but DBP was increased at 1 minute after intubation(P$lt;0.05). and SBP, DBP, MAP & HR were maintained higher level than group I at every time. 4) Group 3; Transtracheal injection of l% lidocaine 2~3 ml; SBP, DBP & MAP were not exceed baseline level at 1 minute but HR was significantly increased at l, 2 minutes after intuhation(P$lt;0.05). Compared with control group, SBP, DBP, and MAP were statistically singnificant (P$lt;0.05). This study suggest that administration of lidocaine attenuate sympathetic stimulation follwing tracheal intubation. Intravenous injection of lidocaine is recommendable method to prevent the sympathetic stimulation following tracheal intubation
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유병식,김병철,임동윤 대한약리학회 2007 The Korean Journal of Physiology & Pharmacology Vol.11 No.1
The present study was designed to establish comparatively the inhibitory effects of cilnidipine (CNP), nifedipine (NIF), and ω-conotoxin GVIA (CTX) on the release of CA evoked by cholinergic stimulation and membrane depolarization from the isolated perfused model of the rat adrenal medulla. CNP (3 μM), NIF (3μM), and CTX (3μM) perfused into an adrenal vein for 60 min produced greatly inhibition in CA secretory responses evoked by ACh (5.32×10-3 M), DMPP (10-4 M for 2 min), McN-A-343 (10-4 M for 2 min), high K+ (5.6×10-2 M), Bay-K-8644 (10-5 M), and cyclopiazonic acid (10-5 M), respectively. For the CA release evoked by ACh and Bay-K-8644, the following rank order of potency was obtained: CNP>NIF>CTX. The rank order for the CA release evoked by McN-A-343 and cyclopiazonic acid was CNP>NIF>CTX. Also, the rank orders for high K+ and for DMPP were NIF>CTX>CNP and NIF>CNP>CTX, respectively. Taken together, these results demonstrate that all voltage-dependent Ca2+ channels (VDCCs) blockers of cilnidipine, nifedipine, and ω-conotoxin GVIA inhibit greatly the CA release evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors and the membrane depolarization without affecting the basal release from the isolated perfused rat adrenal gland. It seems likely that the inhibitory effects of cilnidipine, nifedipine, and ω-conotoxin GVIA are mediated by the blockade of both L- and N-type, L-type only, and N-type only VDCCs located on the rat adrenomedullary chromaffin cells, respectively, which are relevant to Ca2+ mobilization. It is also suggested that N-type VDCCs play an important role in the rat adrenomedullary CA secretion, in addition to L-type VDCCs.
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Depressor action and vasorelaxation of methylene chloride fraction extracted from Rubus coreanum
유병식,최미성,임동윤 대한고혈압학회 2014 Clinical Hypertension Vol.20 No.-
Introduction: The present study was designed to examine whether methylene chloride (CH2Cl2) fraction extracted from Rubus coreanum affects the contractility of the isolated thoracic aortic strips and blood pressure of normotensive rats. Methods: One of the common carotid arteries or of the femoral arteries was catheterized with a polyethylene tubing. The tubing was connected to a pressure transducer, and pulse of the mean arterial blood pressure was recorded on a biological polygraph continuously. Results: The CH2Cl2 fraction (range, 200 to 800 μg/mL) significantly depressed both phenylephrine (PE, 10 μM)- and high K+ (56 mM)-induced contractile responses of the isolated thoracic aortic strips in a concentration-dependent fashion. In the simultaneous presence of Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) (an inhibitor of nitric oxide [NO] synthase, 300 μM) and the CH2Cl2 fraction (400 μg/mL), both PE- and high K+-induced contractile responses were recovered to the significant level of the corresponding control response in comparison with inhibition of CH2Cl2 fraction treatment alone. Moreover, in the simultaneous presence of the CH2Cl2 fraction after pretreatment with 0.4% CHAPS (3-[(3-cholamidopropyl) dimethylammonio]-1-propane sulfonate), both PE- and high K+-induced contractile responses were recovered to the significant level of the corresponding control response compared to the inhibitory response of CH2Cl2 fraction treatment alone. Also, in anesthetized rats, the CH2Cl2 fraction (range, 0.3 to 3.0 mg/kg) injected into a femoral vein dose-dependently produced depressor responses. This hypotensive action of the CH2Cl2 fraction was greatly inhibited after treatment with phentolamine (1 mg/kg), chlorisondamine (1 mg/kg), L-NAME (3 mg/kg/30 min), or sodium nitroprusside (30 μg/kg/30 min). Intravenous infusion of the CH2Cl2 fraction (range, 1.0 to 10.0 mg/kg/30 min) markedly inhibited norepinephrine-induced pressor responses. Discussion: Taken together, these results demonstrate that the CH2Cl2 fraction causes vascular relaxation in the isolated rat thoracic aortic strips as well as hypotensive action in anesthetized rats. These vasorelaxation and hypotension of the CH2Cl2 fraction seem to be mediated at least by the increased NO production through the activation of NO synthase of the vascular endothelium and the inhibitory adrenergic modulation.
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