심포지움 : 약물과 간상해 ; " 약물과 간장 " - 약리학적 견지에서 -

홍사석(Sa Suk Hong) 대한소화기학회 1974 대한소화기학회지 Vol.6 No.1

췌장염의 원인과 치료

홍사석 ( Sa Suk Hong ) 대한내과학회 1967 대한내과학회지 Vol.10 No.3

췌장질환 : 취장의 외분비생리

홍사석 ( Sa Suk Hong ) 대한내과학회 1975 대한내과학회지 Vol.18 No.5

아드레나린성 약물이 유문부결찰 백서의 위분비 기능에 미치는 영향

홍사석(Sa Suk Hong),김학산(Hak San Kim),김예식(Ye Sik Kim),김동구(Dong Goo Kim) 대한소화기학회 1987 대한소화기학회지 Vol.19 No.1

N/A Gastric secretion is modulated largely by three major factors-the autonomic nervous system, the gastrointestinal hormones and the circulation. For autonomic nervous system, the parasympathetic influence on gastric secretion has been widely studied. However, the influence of sympatho-adrenal system has received much less attention and its role on gastric secretion remains a matter of controversy. Present investigation was undertaken to evaluate the adrenergic influence on gastric secretion using the experimental model of pylorus-ligated rat. Immediately after pylorus ligation intrinsic or synthetic adrenergic agents (methoxamine, norepinephrine, epinephrine, isoproterenol or dopamine) were injected subcutaneously. After 3-or 6-hour period of pyloric ligation the stomach was removed and gastric juice was collected for the evaluation of gastric secretory function. And blood glucose level was also measured. The results obtained are as folllows. 1) Gastric secretory function was active in the group of 3 hours pyloric-ligation and depressed greatly therafter. 2) All adrenergic drugs used in this experirnent suppressed the volume of gastric juice and acid output. The degree of suppression was marked in epinephrine or isoproterenol, moderate in methoxamine or norepinephrine and minimal in dopamine treated rats. 3) Blood glucose level was not directly correlated with the suppressive action of adrenergic drugs on gastric secretion. From the above results it is concluded that gastric secretory function is suppressed by adrenergic influence. And it is suggested that adrenergic beta-receptor acitivation plays a major role in the suppression of gastric secretion.

Isoelectric Focusing 법을 이용한 췌효소 단백분리에 관한 실험

홍사석(Sa Suk Hong),김경환(Kyung Hwan Kim),김원준(Won Jun Kim) 대한소화기학회 1972 대한소화기학회 추계학술대회 Vol.1972 No.-

N/A

담즙산류가 담즙배설에 미치는 영향

홍사욱(Sa Uk Hong),박대성(Dae Sung Park),한덕용(Duk Yong Han),이종철(Jong Chul Lee),홍사석(Sa Suk Hong) 대한약학회 1972 약학회지 Vol.16 No.4

The bile secretion was accelerated generally by the administration of all derivatives tested: chemodeoxycholate, deoxycholate, cholate, dehydrocholate, 7-keto-chenodeoxycholate, and 3,7-diketochenodeoxycholate in decreasing order. Bile acids content in bile from animals administered with cholate was increased, however, other derivatives did not alter the contents of bile acids and bilirubin. In view of pharmacological point, all derivatives have hydrocholeretic action, however, only cholate exhibits typical choleretic action.

Studies on the Regulation of Calcium Activity in Myocardial Contraction

고창만,홍사석,Ko, Chang-Mann,Hong, Sa-Suk The Korean Society of Pharmacology 1990 대한약리학잡지 Vol.26 No.2

전기장 자극으로 수축을 유발한 흰쥐 좌심방에서, 자극 빈도 변경에 따른 수축 운동의 변동에 미치는, 여러 경로를 통한 수축 유발 calcium의 영향을 검색하므로, 각 경로가 심근 수축에 미치는 영향을 추구하였다. 흰쥐 좌심방은 자극 빈도를 급격하게 낮추므로, 특징적인 삼단계 변동을 나타내었다. 즉, 처음의 급격한 수축 장력증가와, 두번째 일시적인 빠른 장력감소, 이어서 세번째로 수축장력의 유지단계로 나타났으며, 이때 수축장력은 고빈도 자극시의 2배 정도가 되었다. Caffeine처치는 이와같은 자극빈도 하강에 따른 수축 장력의 증가를 현저하게 억압하였다. Verapamil은 고빈도 자극시 수축 운동을 완전히 소실시켰으나, 저빈도 자극으로 변경시에는 verapamil 존재하에서도 수축 운동이 소생되었다. 한편 ouabain처치나 영양액내 sodium 배제시에는 저빈도 자극으로 나타나는 특징적인 두번째 단계의 변동이 소실되었다. 이러한 결과로 보아, 심근막의 calcium통로는 세포내 유지에 필수불가결한 경로이며, 심근 수축 유발 calcium의 주된 기원은 근 소포체로 부터 유리되는 것으로 믿어진다. 또한 sodium-calcium교환은 세포내 sodium농도의 변동에 따라 수축 유발 calcium양 형성에 조절 인자로서의 기능을 갖는 것으로 추측된다. Influences of trigger calcium on myocardial contraction from several sources were investigated on the frequency reduction-induced changes of contraction in rat left atria driven by electrical field stimulation. Rat atria elicited characteristic three phase-changes according to frequency reduction: the first rapid rise in twitch tension, the second transient fast decrease in tension and the third maintenance of twitch tension at about 200% of resting tension during high frequency. Caffeine treatment enormously suppressed the frequency reduction-induced twitch tension increase. The atrial contraction during high frequency vanished after verapamil treatment. But, during low frequency, atrial contraction revived in the presence of verapamil. Ouabain treatment and sodium depletion in superfusing solution abolished the characteristic second phase with slow frequency. These results suggest that slow calcium channel is an indispensable calcium entry route and calcium release from sarcoplasmic reticulum is an major source for trigger calcium in cardiac contraction. And sodium-calcium exchange has a modulatory roles in the regualtion of trigger calcium according to the changes of intracellular sodium concentration.

Depression of Maternal Immune Response during the Period of Implantation in Rabbits

조혜성,유경자,홍사석,Cho, Hye-Seong,Ryu, Kyung-Za,Hong, Sa-Suk The Korean Society of Pharmacology 1987 대한약리학잡지 Vol.23 No.2

본 실험에서는 가토에서 배반포가 자궁내막에 착상할 때, 모체의 면역기능의 변화를 알아보고, 착상시 관여하는 호르몬과 모체의 면역기능과의 연관성을 관찰하여 다음과 같은 결과를 얻었다. 1. 임신 7일째 가토의 말초혈관 림프구에 concanavalin A를 처리하면, 임신하지 않은 가토의 림프구보다 훨씬 낮은 자극지수를 나타냄으로써 면역억제 현상이 나타나는 것을 관찰할 수 있었다. 2. 임신 7일 때의 혈청 progesterone농도인 11.56 ng/ml을 임신하지 않는 가토의 말초혈관 림프구에 처리하면, 억제현상을 나타내지 않았으나, Progesterone의 농도가 1000 ng/ml 이상에서는 농도에 비례하여 림프구의 활성도가 감소되었다. 3. 4.5 ng/ml${\sim}$4,500 ng/ml의 $PGF_{2{\alpha}}$는 concanavalin A처리시 림프구의 활성도에 별다른 영향을 끼치지 않았으나, PGE는 4.5 ng/ml${\sim}$4,500 ng/ml에서 농도에 비례하여 림프구의 활성도를 유의하게 감소시켰다. 그러나 임신 제 8일째의 말초혈관 림프구에 prostaglandin 합성 억제제인 indomethacin 0.1 또는 $1\;{\mu}g/ml$을 처리하면 억제되었던 림프구 활성도가 각각28%, 23% 증가되었다. 이상의 결과로 보아 토끼의 착상기간중 모체의 면역기능이 저하되며 PGE가 착상기간중 면역기능을 저하시키는 요소중 하나인 것으로 생각된다. We determined the maternal peripheral lymphocyte response to mitogen during the period of implantation and evaluated the effects of hormones, which are known to be involved in the process of implantation, on the lymphocyte activity in rabbits. As compared with peripheral lymphocyte activity in non-pregnant rabbits, lymphocyte activity was significantly depressed on days 6, 7 and 9 of pregnancy. Although concentrations of serum progesterone were gradually increased during the implantation period, progesterone did not inhibit lymphocyte activity at physiological concentration. Serum $PGF_{2{\alpha}}$ was significantly increased on day 7 while PGE was slightly increased. $PGF_{2{\alpha}}$ did not modify lymphocyte activity even with greater concentrations than physiological level. However, lymphocyte activity was significantly inhibited by PGE even with physiological doses. The treatment of indomethacin at doses of 0.1 or $1.0\;{\mu}g/ml$ tended to enhance lymphocyte response, which was depressed on day 8 of pregnancy, 28% or 23% respectively. Although in non-pregnant rabbit, enhancement of lymphocyte response was also shown after the treatment of indomethacin, this enhancement was much less than that in pregnant rabbits. These results strongly suggest that maternal immune response was depressed during the process of implantation and PGE might be one of factors for immunomodulation during this period.

Aminoglycosides의 취효소 분비항진기전에 관한 연구

심호식,김경환,홍사석,Shim, Ho-Shik,Kim, Kyung-Hwan,Hong, Sa-Suk 대한약리학회 1983 대한약리학잡지 Vol.19 No.1

Aminoglycoside antibiotics are reported to enhance the amylase release from isolated slices of pancreas in vitro and the mode of action of aminoglycosides on amylase release is considered different from those of acetylcholine or cholecystokinin(CCK), i.e., electronmicroscopically intact zymogen granules are appeared in the lumen of pancreatic acini by treatment of aminoglycosides. It is known that atropine blocks the secretagogue effect of acetylcholine, and phenoxybenzamine is reported to block the effects of CCK or its analogue caerulein. Present study was undertaken to investigate the mode of action of aminoglycosides on the amylase release using atropine, phenoxybenzamine and propranolol as a membrane stabilizing agent in slices of chicken pancreas. The results are summarized as follows : 1) Streptomycin and kanamycin increased the amylase release significantly from slices of chicken pancreas. 2) The effect of streptomycin was inhibited by atropine but not by phenoxybenzamine or propranolol. 3) The amylase release by acetylcholine was blocked by atropine tut the effect of cholecystokinin octapeptide(CCK-8) was not influenced by atropine, phenoxybenzamine or propranolol. 4) Pretreatment of streptomycin enhanced the secretagogue effect of acetylcholine or CCK-8. From these results it is suggested that amylase releasing effects of aminoglycosides are mediated in part by cholinergic stimulation and in part by membrane alteration and these effects are enhanced by acetylcholine or cholecystokinin.

뇌실내 Calcitonin 투여가 위산분비에 미치는 영향에 관한 연구

최흥재(Heung Jai Choi),홍사석(Sa Suk Hong),김경환(Kyung Hwan Kim),이상인(Sang In Lee),권상옥(Sang Ok Kwon),안영수(Young Soo Ahn),장우익(Woo Ick Jang),연규홍(Kyu Hong Yeon),고창만(Chang Mann Ko) 대한소화기학회 1989 대한소화기학회지 Vol.21 No.4

N/A Peptides that are common to the brain and gut are thought to plav intermediary roles as neurotrans- mitters or neuromodulators in the regulation of gut function. Calcitonin is a polypetide hormone of 32 amino acid residues. Intracerebroventricular (ICV) administration of calcitonin does not alter plasma calcium or phosphorus concentrations. Recently, much evidence is accumulating to suggest that calcitonin may inhibit gastric acid secretion by a central action. But the neurohumoral pathways mediating antitsecretory effects of calcitonin in rats are not well elucidated. In the present study, using a gastric perfusion technique, effects of ICV administration of calcitonin on gastric acicl secretion and stress ulceration and its mechanism were investigated in rats. The results obtained are as follows: 1) ICV administration of calcitonin suppressed basal gastric acid secretion in a dose-dependent manner. 2) Gastric acid secretion stimulated by histamine, bethanechol or pentagastrin was not suppressed by ICV administration of calcitonin. 3) Gastric acid secretion stimulated by TRIl was markedly suppressed by ICV administratioti of calcitoninl. 4) Bilateral vagotomy did not influence calcitonin-induced gastric acid suppressionl. 5)Pretreatment metyrosine did not itnfluence cailcitoinin-induced gaitric acid suppression. 6) Intravenous administration of high dose (25 IU) of calcitonin suppressed gastric acid secretion. Central administration of calcitonin was approximately 250 times more sensitive than intravenous administration. 7) Stress ulcers induced by cold restraint and TRH administration were diminished by ICV admitnistration of calcitonin. In this study it is demonstrated that calcitonin suppresses gastric acid secretion, and this inhibitory effcct is centrally mediated. In particular, calcitonin suppresses TRH induced gastric acid secretion and stres ulcer formation. And it is suggested that calcitonin seems to play an inhibitorv role in gastric acid secretion as a neuromodulator in the central nervous system.