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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.
L - Asparaginase 의 취독성에 대한 실험적 검토
홍사석 ( S. S. Hong ),김원준 ( W. J. Kim ),김경환 ( K. H. Kim ),김혜경 ( H. K. Kim ),김정숙 ( C. S. Kim ),김대현 ( D. H. Kim ),이용우 ( Y. W. Lee ) 대한내과학회 1973 대한내과학회지 Vol.16 No.8
Toxic effect of L-asparaginase(NSC 109229, Merck Sharp & Dohme) on pancreas after single repeated administration was studied in rabbits and rats. Rectal temperature was slightly elevated in rabbits at one hour after intravenous administration of L-asparagi
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.
Cholecystokinin-pancreozymin의 식도절편 수축반응에 미치는 phenoxybenzamine의 영향
조태정,김원상,홍사석,Cho, T.S.,Kim, W.J.,Hong, S.S. 대한약리학회 1980 대한약리학잡지 Vol.16 No.1
In this study, the effects of phenoxybenzamine and related drugs on the action of CCK-PZ and caerulein were examined in isolated gall bladder of guinea pig and higher esophagus strip of fowl. The strips were placed in a bath containing Locke-Ringer solution maintained at $38^{\circ}C$. Oxygen was continuously bubbled through the solution. The contractile response was measured isometrically by a force displacement transducer connected to polygraph. In isolated gall bladder preparation caerulein produced contractile response of CCK-PZ type, but the relative potency on a weight basis was 30 times stronger than CCK-PZ. The response of caerulein or CCK-PZ was not blocked by cholinergic blocking agent and both alpha and beta adrenergic blockades, however, the response of caerulein or CCK-PZ was exceptionally blocked by phenoxybenzamine. In isolated esophagus strip CCK-PZ with high concentration produced marked contraction which was not modified by atropine and other blocking agents, whereas the response was blocked by phenoxybenzamine. These results lead to the conclusion that phenoxybenzamine inherently inhibits the contractile response of CCK-PZ and caerulein on esophagus and other smooth muscle.