Effect of Atropine and SC-15396 on Stimulated Gastric Acid Secretion in the Atlantic Cod,Gadus morhua

Gastric acid secretion was measured in swimming codfish surgically equipped with a catheter draining the stomach. Gastric acid secretion was stimulated by histamine (5 or 15μg/kg-h) or by carbachol (5μg/kg-h). Pretreatment with atropine (1 μmol/kg-h) completely prevented the acid secretion induced by carbachol, but did not influence the secretion induced by histamine. Atropine had marked effects on the motor functions of the stomach, and seriously reduced the volume draining from the stomach. Infusion of phenol red indicated that the decrease in volume was due to a decrease in recovery of ingested water. SC-15396, “antigastrin”, significantly depressed acid secretion induced by histamine, and reduced carbachol-stimulated secretion, although the latter was statistically insignificant. The effects of SC-15396 is discussed with reference to the absence of receptors for gastrin related to gastric acid secretion in the codfish stomach.     

Subfornical organ neurons with efferent projections to the hypothalamic paraventricular nucleus: an electrophysiological study in the rat

Seventeen neurons in the subfornical organ (SFO) were antidromically activated by electrical stimulation of the paraventricular nucleus (PVN) in the rat. The activity of all identified SFO neurons was excited by microiontophoretically (MIPh) applied angiotensin II (AII) and the effect of AII was blocked by MIPh-applied saralasin (Sar), an AII antagonist, but not by atropine (Atr), a muscarinic antagonist. In these identified SFO neurons, 9 were also excited and 8 were not affected by MIPh-applied acetylcholine (ACh) and the effect of ACh was attenuated by not only MIPh-applied Atr but also by Sar. These results suggest that there are specific AII- and both AII- and ACh-sensitive types of SFO neurons with efferent projections to the PVN.     

抗菌药物和654—2对缺血性肠粘膜的保护作用

采用大鼠肠缺血模型，观察了肠缺血早期肠道内应用用抗菌药物并肌注６５４－２的效应。结果发现，治疗组大鼠肠粘膜、肝、肾、肺脏的损害程度较实验组明显减轻，肠道细菌转移率下降（Ｐ〈０．０１），动物生存时间延长（Ｐ〈０．０１）；提示：本方案对缺血性肠粘膜及脏器组织具有一定的保护作用。     

Monoamine replacement after reserpine: Catecholaminergic agonists restore motor activity but phenylethylamine restores atropine-resistant neocortical low voltage fast activity

A large dose of reserpine abolishes an atropine-resistant form of neocortical low voltage fast activity (LVFA) which normally accompanies certain patterns of motor activity in rats. An attempt was made to reverse this effect by replacement of specific monoamines or by injection of suitable agonists in rats pretreated with reserpine (10 mg/kg). The following compounds, alone or in various combinations, failed to restore atropine-resistant LVFA in reserpinized rats even though spontaneous motor activity was restored in many cases: l-DOPA (150–300 mg/kg) after pretreatment with an inhibitor of peripheral l-aromatic amino acid decarboxylase; 5-hydroxytryptophan (100–200 mg/kg); d-amphetamine (1–2 mg/kg); apomorphine (0.25–2.5 mg/kg); lysergic acid diethylamide (100–300 g/kg); and clonidine (0.5–1.0 mg/kg). In contrast β-phenylethylamine was quite effective in restoring atropine-resistant LVFA and its effects were not diminished by pretreatment with α-methyl-p-tyrosine (400 mg/kg), chlorpromazine (15 mg/kg) or trifluoperazine (5–10 mg/kg). It is suggested that a trace amine plays an essential role in the production of atropine-resistant LVFA independent of catecholamines.     

Response of the whole bladder-urethra model (rabbit) to autonomic drugs

To investigate the function of the bladder-urethra as a continuous unit we set up an in vitro whole bladder-urethra model (rabbit). We were able to measure the intravesical pressure at which saline infused into the bladder emptied via the urethra (“opening pressure”). Methoxamine added to the bath caused a significant increase in opening pressure, whereas phentolamine caused a significant decrease in opening pressure compared to controls. Atropine had no effect on opening pressure in the absence or presence of methoxamine. Thus, it appears that the in vitro bladder-urethra unit has intrinsic alpha-adrenergic tone that is of sufficient force to maintain an intravesical pressure of 7.0 cm H₂O, and that this tone is not influenced by antagonism with the anticholinergic agent atropine.     

Plasma levels of somatostatin following a test meal in dogs Initial atropine resistant vagally mediated decrease of somatostain levels and increase of gastrin and insulin levels

Plasma levels of somatostatin like immunoreactivity (SLI), below referred to as somatostatin levels, were measured in peripheral plasma of conscious dogs. Basal somatostatin levels averaged 49±10 pM. Somatostatin as well as gastrin and insulin plasma levels were measured before and after feeding with and without prior atropinization. During the first 10 min after feeding somatostatin levels fell from 49±10 to 23±9 pM, whereas gastrin and insulin levels rose from 9±2 and 140±14 pM to 48±11 and 370±91 pM respectively. Atropine 0.01 or 0.1 mg/kg did not inhibit these responses. After the initial decrease, somatostatin levels rose again and peaked at around 60 min after feeding (110±24 pM). This secondary rise was completely abolished by atropine in both doses tried. Gastrin and insulin levels remained elevated throughout the experiments with and without atropine. It is suggested that gastrin release and HCI secretion are inhibited by a tonic outflow of gastric somatostatin during basal conditions. The process of feeding induces an atropine resistant, vagally mediated decrease in somatostatin release from the gastrointestinal tract and this decreased output of somatostatin facilitates initiation of meal-related endocrine and exocrine gastric secretions.     

5—羟色胺M受体和胆碱能受体阻断剂在红霉素所致小肠动力紊乱和呕吐中的作用

本实验对８条犬进行小肠肌电测定，并在记录期间分别静注胆碱能神经阻断剂，阿托品和六甲季胺，以及５－羟色胺（５－ＨＴ）Ｍ受体阻断剂，灭吐灵，以观察其对红霉素所致肠道副作用的影响。结果发现阿托品和六甲季胺不仅能明显地抑制空腹时正常传播性肌电综合波（ＭＭＣ）的发生和传播，降低红霉素促进小肠动力的作用，还能减轻红霉素所致饱腹动物的快波数增加，但对呕吐无明显影响。灭吐灵的实验结果显示红霉素的致吐作用是由５－ＨＴＭ受体介导的，与其促进小肠动力的作用无明显因果关系。