To see if the treatments of d-amphetamine and chlorpromazine have any influence upon the orienting response and general behavioral activity, 3 groups of male Holtzman rats were prepared, namely d-amphetamine animals (1.0 mg/kg.i.p.), chlorpromazine rats (1.0 mg/kg.i.p.) and the physiological saline control animals. The general behavioral activity was examined by visual scanning using the time-sample method in the adaptation period of orienting response. The occurence of orienting response and its rate of habituation were evaluated by observing cessation of ongoing activity in response to a sound stimulus (1,000 Hz, 70 db & 0.1 sec), or turning of head toward the source of stimulus in 20 trials. Attention shift from sound to light stimulus was also tested in 10 trials. The results obtained were as follows; 1. The general behavioral activity of d-amphetamine group was significantly greater than that of control, however, the chlorpromazine animals showed the tendency to decrease in activity. 2. The d-amphetamine group showed the occurence of orienting response to sound significantly more often than that of placebo controls. However, the chlorpromazine group exhibited significantly fewer orienting response than the placebo group did. 3. The d-amphetamine group displayed no clear out habituation to the orienting response following the repetition of trials, though the placebo and the chlorpromazine groups demonstrated apparent habituation to the response. 4. The three animal groups did not differ significantly from each other with regard to shift of attention from sound to light stimulus. It is inferred that the d-amphetamine tends to increase general activity has a definite facilitative action of orienting response and a inhibitory influence upon the habituation of the latter response. On the contrary, the chlorpromazine tends to decrease general activity, has a inhibitory action of orienting response and facilitatory action of habituation of the response.

Certain metabolic aspects of halothane's cardiac depressant action on the contractility of the myocardium were elucidated from a sudy of the effect of pyruvate on halothane-depressed rat atria. Approximately 6 mg% halothane was required to maintain a 50% depression of the contractility of rat atria suspended in a modified Krebs-Ringer bicarbonate glucose medium, pH 7.4, $30^{\circ}C$ for a 2 hr. period. Pyruvate was found to restore partially the contractility of halothane-depressed atria. The maximally effective concentration of pyruvate was 2.5 mM. There was minimal pyruvate effect on the force of contraction of control atria. The effect of pyruvate on halothane-depressed atria was shown to be due to the pyruvate and not the sodium ion of the sodium pyruvate. Pyruvate was found to produce no increase in the contractility of atria depressed by hypertonic medium, but caused a further depression. Selected aspects regarding the action of halothane on glucose metabolism in myocardial cells are discussed. The results are consistent with the hypothesis that at least a part of the negative inotropic action of halothane is due to an inhibition of glucose uptake or utilization in the glycolytic pathway.

기니아-픽 및 백서정관(白鼠精管)에 대(對)한 $PGE_1$의 작용(作用)과 이들 조직(組織)에 있어서 교감신경효능제(交感神經效能劑)의 작용(作用)에 미치는 $PGE_1$의 효과(效果)를 보고 나아가서 계양막(鷄羊膜)에 대(對)한 $PGE_1$의 작용(作用)을 관찰(觀察)하였다. 1. 기니아-픽 적출정관표본(摘出精管標本)에서 $PGE_1$전처치(前處置)에 의(依)하여 phenylephrine이나 norepinephrine의 작용(作用)이 증강(增强)되었으며, 하복신경(下腹神經)-근표본(筋標本)에서 신경자극(神經刺戟)이나 trans-mural stimulation에 의(依)한 수축(收縮)에 미치는 phenylephrine, norepinephrine 및 tyratnine의 작용(作用)이 $PEG_1$ 전처치(前處置)에 의(依)하여 증강(增强)되었다. 특히 긴장상승(緊張上昇)이 현저(顯著)하였다. 2. 백서정관(白鼠精管)의 하복신경(下腹神經)-근표본(筋標本)에서는 기너아-픽 정관(精管)에서와는 달리 $PGE_1$을 처리(處理)함으로써 신경자극(神經刺戟) 및 transmural stimulation에 의(依)한 수축고(收縮高)가 서서(徐徐)히 감소(減少)되고, $PGE_1$을 전처치(前處置)한 후(後)에도 $10^{-6}g/ml$ phenylephrine 또는 norepinephrine에 의(依)한 긴장상승(緊張上昇)이나 수축고(收縮高)의 증가(增加)는 나타나지 아니 하였다. 3. 신경섬유(神經纖維)가 제거(除去)된 기니아-픽정관(精管)에 있어서는 $PGE_1$ 전처치(前處置)에 의(依)하여 phenylephrine 또는 norepinep. hrine의 작용(作用)이 증가(增加)되나 denervation 된 백서(白鼠)의 정관(精管)에 있어서는 $PGE_1$ 처리(處理)로서는 norepinephrine의 작용(作用)에 하등(何等)의 영향(影響)을 주지 아니 하였다. 4. 계양막평활근(鷄羊膜平滑筋)의 자발운동(自發運動)은 저농도(低濃度) $PGE_(10^{-8}g/ml)$에 의(依)하여 거의 변화(變化)를 받지 아니 하나, 농도(濃度)가 增加(增加)함으로서 자발운동(自發運動)은 불규칙(不規則)하나 대체(大體)로 억제적(抑制的)으로 나타났었고, $PGE_1$ 전처치후(前處置後) 고농도(高濃度) phenylephrine을 작용(作用)시켰으나 구등(?等)의 영향(影響)을 받지 아니 하였고 physostigmine의 작용(作用)은 길항(拮抗하였다. 이상(以上)의 결과(結果)로 보아 $PGE_1$은 동물(動物)의 정관(精管)에 대(對)한 작용(作用)에는 종(種)의 차이(差異)가 있으며 $PGE_1$은 교감신경효능제(交感神經效能劑)에 의(依)한 기니아-픽 정관수축작용(精管收縮作用)에 대(對)하여 supersensitivity를 야기(惹起)시켰으며, 이는 정관평활근(精管平滑筋)에 대(對)한 직접작용(直接作用)이 아닌 다른 작용기전(作用機轉)에 기인(基因)할 것으로 사료(思料)되는 바이다.

Krebs-Ringer bicarbonate 완충용액(pH 7.4, 4%(w/v) bovine serum albumin 함유)에 백서부고환지방조직을 incubation 하면서 FFA 유리에 대한 인삼 saponin의 작용을 관찰한 saponin 농도 1mg/ml에서 FFA의 유리가 현저히 증가되었으며 0.01mg/ml에서는 오히려 감소하였다. Epinephrine으로 전처치하여 hormone-sensitive lipase system을 활성화시킨 백서부고환지방조직 homogenate에서는 $0.1{\sim}1mg/ml$의 인삼 saponin에 의하여 FFA 동원이 현저히 증가하였으며 0.01mg/ml에서는 역시 감소하였다. 유효농도에서의 인삼 saponin은 epinephrine에 의한 지방조직으로 부터의 FFA 동원에 아마도 협동적으로 작용할 것으로 사료된다.

The isolated rabbit gall bladder strips were prepared according to the technique described by Amer and Becvar (1969). The strips were placed in a bath containing 100 ml of Locke-Ringer solution maintained at $38^{\circ}C$. Oxygen was continuously bubbled through the solution. The tension of the muscle strip was initially adjusted to 0.7g. The contractile response was measured isometrically by a force-displacement transducer connected to a polygraph. The effect of a number of autonomic drugs were studied for their interaction with caerulein (Prof. V. Erspamer, F.I. 6934 Caerulein, Farmitalia, Italia), a gastrin or CCK.PZ like peptide, on isolated rabbit gall bladder strips. In this preparation caerulein produced contractions of CCK-PZ type, but the relative potency on a weight basis was 40 times that of CCK-PZ. The response of caerulein was not modified by either cholinergic or alpha or beta adrenergic blockade. However, the response of caerulein and of barium on the strips were prevented by papaverine or aminophylline. Isoproterenol, papaverine or aminophylline alone relaxed the preparation whereas caerulein, CCK-PZ, acetylcholine, serotonin, histamine or barium chloride contracted the preparation. In summary, it is concluded that caerulein on the gall bladder strip seems to act independently of the autonomic nervous system and mediated via mechanisms apparently similar to those involved in the action of barium chloride.

Further elucidation of the mechanism of halothane's negative inotropic action has resulted from a study of the effect of various substrates on halothane-depressed rat atria. Approximately 6 mg% halothane was required to maintain a 50% depression of the contractility of rat atria suspended in a modified Krebs-Ringer bicarbonate glucose medium, pH 7.4, $30^{\circ}C$ for 2hr. Both lactate and acetate were found to restore partially the contractility of halothane-depressed atria. The maximally effective concentration of lactate was 5 mM; for acetate it was 2.5mM. Neither 5 nor 20 mM of additional glucose was effective in restoring the force of contraction of halothane-depressed atria. The results are consistent with the hypothesis that halothane exerts at least a part of its negative inotropic effect on rat atria by inhibiting either the uptake or utilization of glucose by the myocardium. The site of blockade must be prior to the conversion of pyruvate to acetyl CoA. In our previous report dealing with the mechanism of cardiac depressant action of inhalation anesthetic halothane, it has been demonstrated that: 1) approximately 6 mg/100 ml halothane is required to maintain 50% depression of the force of contraction of isolated rat atria in Krebs-Ringer bicarbonate glucose medium; 2) pyruvate partially restores the contractility of halothane-depressed atria, but has no effect on normal atria; the partial recovery of depressed atria by the addition of sodium pyruvate is due to the effect of the pyruvate ion itself, not to the sodium ion; 4) addition of pyruvate, to atria depressed with hypertonic medium, produced only further depression. From these findings we concluded that the cardiac depressant action of halothane on rat atria is a manifestation of inhibition of glucose uptake or utilization. The present studies were undertaken to observe the effect of other substrates on halothane-depressed atria in order to substantiate our conclusion. As with the case of pyruvate, lactate and acetate also partially restored the force of contraction of halothane-depressed atria. These data are consistent with the hypothesis that halothane inhibits glucose uptake or utilization in the glycolytic cycle of the myocardium.

Berberis koreana Palibin belonging to Berberidaceae family, a common herb in Korea, has been contained some quantity of Berberine analogue and other ingredients. Authors therefore paid attention to its pharmacological actions and examined the effects on sleep duration and rectal temperature in mouse with crystal (A) from Berberis koreana Palibin in Korean native plans. The experiment searching for the effect on sleep duration was performed with pretreatment of Berberis Koreana Palibin crystal (A) 30 min before the administration of 25 % ethanol, and its crystal were also administered intraperitoneally with the intention to examine the effect on rectal temperature in mouse. The results of the experiment were as follows; 1. Crystal (A) from Berberis koreana Palibin was made by extraction with ethanol and HCI. 2. Crystal (A) enhanced the hypnotic activity of alcohol in concentratins of 0.1 mg/10g or 0.15 mg/10g. 3. Rectal temperatures in mice were significantly reduced with administration of crystal (A) in concentrations of 0.1 mg/10g or 0.15 mg/10g. 4. The maximal reduction of rectal temperature and potentiation of the hypnotic activity were observed at 30 min after its administration. From the above results, it is clear that crystal (A) from Berberis koreana Palibin exerts the potentiation of hypnotic action of alcohol and reduction of rectal temperature in normal mouse. Its pharmacological effects are probably derived from the action upon the central nervous system.