刺激家兔额叶皮层影响尾核痛单位放电机制的初步探讨

目的：探讨额叶皮层对尾核痛单位放电的影响及其可能机制。方法：参照Ｓａｗｙｅｒ兔脑图谱，用ＳＮ－２型推进器以２μｍ／ｓ速度将玻璃微电极插入尾核头部Ａ３～５，Ｒ３．５～５，Ｈ３．５～５处引导神经元自发放电。结果：引导了尾核单位放电３７９个，其中痛单位８６个，占引导总数的２２．６８％，包含痛兴奋单位（ＰＥＮ）５７个，占痛单位的６６．２８％；痛抑制单位（ＰＩＮ）２９个，占３３．７２％。尾核有７４．４２％的痛单位对刺激额叶皮层起反应。刺激额叶皮层可易化尾核ＰＩＮ的电活动（６２．５２％出现增频反应），抑制ＰＥＮ的电活动（６４．９１％出现减频反应）。脑室注射阿托品或氟哌啶醇均可不同程度的阻断刺激额叶皮层对尾核痛单位的影响。结论：额叶皮层参与对尾核痛单位的调制，乙酰胆碱，多巴胺及相应的受体可能参与其调制过程     

褐藻氨酸对M-胆碱受体的作用

本文以离体豚鼠回肠作标本,乙酰胆碱作对照剂,阿托品作对抗剂,观察了褐藻氨酸对肠管平滑肌的作用。结果表明,褐藻氨酸使汤平滑肌产生了剂量依赖性的兴奋作用,该作用可被阿托品竞争性对抗。褐藻氨酸的PD_2为3.86,阿托品的PA_2为9.6.提示褐藻氨酸对M-胆碱受体有激动作用。     

Autoradiographic identification of muscarinic receptors in human iris smooth muscle

We have used the specific, irreversible muscarinic ligand [³H]-propylbenzilylcholine mustard to localize putative muscarinic cholinergic receptors in the smooth muscle tissue of the human iris. Analysis of autoradiograms from labeled irides reveals high grain densities over the iris sphincter muscle, consistent with the well-known pharmacology of this muscle. In addition, a smaller but significant population of muscarinic binding sites was seen in the iris dilator muscle as well. Grain densities in both muscles are substantially reduced in control tissue treated with relatively high concentrations of the muscarinic antagonists quinuclidinyl benzilate (QNB) and atropine. This is, to our knowledge, the first report of autoradiographic localization of putative muscarinic receptors in the human iris.     

Mechanisms of late decelerations in the fetal heart rate. A study with autonomic blocking agents in fetal lambs.

Fetal heart rate decelerations resembling the late deceleration FHR pattern were produced in fetal sheep by periodic occlusion of the maternal common hypogastric artery for 30-60 sec. Transient fetal hypertension also occurred during the occlusions. Alpha-adrenergic blockade with phentolamine eliminated or markedly reduced the hypertensive response. FHR decelerations still occurred intermittently with some occlusions; however, their character was greatly altered. After parasympathetic blockade with atropine, the decelerations were replaced by periodic FHR accelerations during the occlusions. These accelerations were, in turn, eliminated by the beta-adrenergic blocking agent, propranolol. In the presence of combined parasympathetic, alpha- and beta-adrenergic blockade, the FHR remained essentially constant during the hypogastric artery occlusions in non-acidemic fetuses. FHR decelerations persisted after parasympathetic or total autonomic blockade when the fetuses were significantly hypoxic, as judged by depressed arterial blood pH and base excess values. Beat-to-beat variability of the baseline FHR persisted in the face of severe hypoxia and acidosis. These observations demonstrate that reflex mechanisms are involved importantly in the genesis of late deceleration FHR patterns in the acutely hypoxemic fetus, but that direct depression of myocardial rhythmicity becomes a factor as hypoxic acidosis develops.     

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.     

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.