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PubMed1983

Long-lasting hypersensitivity to methamphetamine following amygdaloid kindling in cats: the relationship between limbic epilepsy and the psychotic state.

This study attempts to analyze the biological mechanisms involved in the association of a psychotic state with temporal lobe epilepsy, and the inverse relation between the epilepsy and this psychotic state. Responses to a test dose of methamphetamine (MAP) were examined in amygdaloid-kindled cats. It was found that (i) MAP-induced stereotyped behavior was enhanced after amygdaloid kindling, and this hypersensitivity lasted for at least 10 days after the final convulsion, (ii) autonomic responses to MAP including piloerection, salivation, heart rate, and respiration rate were also enhanced by the kindling, (iii) kindled generalized convulsions were suppressed during MAP-induced stereotyped behavior in some cats, and (iv) this suppression was blocked by pretreatment with pimozide. Engel and Ackermann proposed that inhibitory events precipitated by each kindling stimulus could produce changes in the catecholaminergic system similar to the reverse tolerance seen with dopamine agonists, and that inhibitory hypersensitivity could parallel the development of kindled excitation. This was partially confirmed by the present study, and leads to the hypothesis that excitation of seizure-inhibiting activity, including activity of the dopamine system, may be related to the emergence of a psychotic state, and to the inverse relationship between epilepsy and the psychotic state in temporal lobe epilepsy.

Amygdala↗
PubMed1982

Transswitching in the treatment of obesity.

Transswitching is a variant of classical conditioning that entails the use of tonic stimuli of relatively long duration in addition to briefer, phasic stimuli which are paired or not paired with the unconditioned stimulus. The same conditioned stimulus can be conditioned to different conditioned responses in different environmental contexts. Using the transswitching procedure, the salivary response to food cues in two obese subjects was modified. The switching agent determined the relative amount of salivation. Techniques that alter alimentary responses to environmental food cues may be helpful in the treatment of obesity.

Adult↗
PubMed1980

Studies on the putative anticholinergic effects of desmethylimipramine.

Desmethylimipramine (DMI) and atropine were compared in a variety of organ system tests in rats and mice involving muscarinic receptor function in order to assess the anticholinergic-like activity of this tricyclic antidepressant drug. DMI was similar to atropine in maximally inhibiting basal gastric acid secretion and markedly protecting against restraint-induced stomach ulceration. It did not, however, substantially increase pupil size, reduce fecal pellet output, inhibit cholinergically induced salivation or specifically antagonize the CNS effects of carbachol and oxotremorine as did atropine. From these data and previous work indicating that DMI acts at a site in the central nervous system to inhibit gastric acid secretion, it is concluded that the biological effects of this drug are not mediated through an atropine-like mechanism.

Animals↗
PubMed1995

Cue-exposure to alcohol-associated stimuli reduces autonomic reactivity, but not craving and anxiety, in dependent drinkers.

A controlled trial was conducted of cue-exposure with dependent drinkers in treatment. All subjects were engaged in an insight-oriented therapy programme, and responses to an alcohol-associated, compared with a neutral, stimulus were assessed at the beginning and end of treatment. Compared with a control group, which did not receive intervening cue-exposure sessions, subjects who received such interventions manifested reductions in heart rate, salivation and arousal responses to the alcohol-associated, compared with the neutral, stimulus. They did not, however, show similar reductions in subjective estimates of craving and anxiety. These results and the desynchrony in reductions in cue-reactivity across response domains are discussed in terms of their implications for cue-exposure in treatment and recent theorectical conceptualizations of the relationship between autonomic reactivity, craving and drinking behaviour.

Adult↗
PubMed1995

[Single administration toxicity studies of T-3761 in mice, rats and dogs].

Single dose toxicity studies of T-3761 were carried out in mice, rats and dogs, and the following results were obtained. 1. The approximate lethal dose of T-3761 were more than 5,000 mg/kg for mice and rats, more than 2,000 mg/kg for dogs with oral administration, and more than 5,000 mg/kg for mice and rats with subcutaneous injection. LD50 values with intravenous injection were 783 mg/kg for male mice, 832 mg/kg for female mice, 341 mg/kg for male rats, and 403 mg/kg for female rats. Two dogs given 200 mg/kg did not die but one of the two treated with 400 mg/kg died after intravenous injection. The approximate lethal dose for dog was 400 mg/kg. 2. Neither abnormal symptoms and macroscopic findings nor deaths were observed in mice and rats treated orally. Granuloma around precipitates of T-3761 at the injection site was seen in mice and rats injected subcutaneously. Slight increase of white blood cell count, serum GOT, CPK and urea nitrogen were transiently found in dogs treated orally. Neither abnormal macroscopic findings nor deaths were observed in dogs treated orally. 3. Decreased motor activity and irregular breathing were observed in mice and rats injected intravenously. In dying animals, tonic or clonic convulsions were observed. Vomiting, hyperemia of ophthalmic mucosa, edema of face, decrease of motor activity, salivation and decrease in body temperature were observed in dogs injected intravenously. At higher doses, scream and tachypnea were observed while injecting. Hematological examinations disclosed that increases in red blood cell count, white blood cell count, hematocrit and hemoglobin were found transiently. In biochemical examinations, increases in serum GOT, GPT, urea nitrogen and creatinine were found transiently. One dog intravenously injected 400 mg/kg, showed tonic convulsion and died.

Animals↗
PubMed1995

Behavioral and electroencephalographic properties of duloxetine (LY248686), a reuptake inhibitor of norepinephrine and serotonin, in mice and rats.

Duloxetine is a dual inhibitor of norepinephrine and serotonin reuptake. Duloxetine (3.13-50 mg/kg p.o.) significantly prevented tetrabenazine (1 and 50 mg/kg s.c.)-induced ptosis in mice and rats. Moreover, duloxetine (1.56-12.5 mg/kg p.o.) also inhibited reserpine (1 mg/kg s.c.)-induced hypothermia in mice. When duloxetine (12.5-100 mg/kg p.o.) and 5-hydroxytryptophan (80 and 100 mg/kg i.p.), a precursor of serotonin, were administered simultaneously to mice and rats, head movement behavior and tremor were observed. In addition, duloxetine (25-100 mg/kg p.o.) significantly attenuated immobility in forced swimming in mice, as equally effective as commonly used antidepressant drugs. Duloxetine (12.5-25 mg/kg p.o.) significantly decreased rapid eye movement sleep and slow-wave deep sleep and increased the awake period, as shown in the rat EEG. However, duloxetine (25-200 mg/kg p.o.) did not affect salivation and lacrimation induced by oxotremorine (1 mg/kg s.c.), a cholinergic agonist, whereas it (25-50 mg/kg) reduced the oxotremorine-induced tremor in part. These results indicated that duloxetine produced behavioral and electroencephalographic responses resulting from the inhibition of norepinephrine and serotonin reuptake in vivo, and that it had a weak anticholinergic action. Therefore, duloxetine may be clinically useful as an antidepressant.

5-Hydroxytryptophan↗
PubMed1994

Xanomeline: a novel muscarinic receptor agonist with functional selectivity for M1 receptors.

Xanomeline [3(3-hexyloxy-1,2,5-thiadiazol-4-yl)-1,2,5,6-tetrahydro-1- methylpyridine] has been evaluated as a muscarinic receptor agonist. In vitro, xanomeline had high affinity for muscarinic receptors in brain homogenates, but had substantially less or no affinity for a number of other neurotransmitter receptors and uptake sites. In cells stably expressing genetic m1 receptors, xanomeline increased phospholipid hydrolysis in CHO, BHK and A9 L cells to 100, 72 and 55% of the nonselective agonist carbachol. In isolated tissues, xanomeline had high affinity for M1 receptors in the rabbit vas deferens (IC50 = 0.006 nM), low affinity for M2 receptors in guinea pig atria (EC50 = 3 microM), was a weak partial agonist in guinea pig ileum and was neither an agonist nor antagonist in guinea pig bladder. In vivo, xanomeline increased striatal levels of dopamine metabolites, presumably by acting at M1 heteroreceptors on dopamine neurons to increase dopamine release. In contrast, xanomeline had only a relatively small effect on acetylcholine levels in brain, indicating that it is devoid of actions at muscarinic autoreceptors. In the gastrointestinal tract, xanomeline inhibited small intestinal and colonic motility, but increased small intestinal transmural potential difference. In contrast to the nonselective muscarinic agonist oxotremorine, xanomeline did not produce salivation, tremor nor hypothermia; it did, however, increase heart rate. The present data are consistent with the interpretation that xanomeline is a novel muscarinic receptor agonist with functional selectivity for M1 muscarinic receptors both in vitro and in vivo.

Animals↗
PubMed1994

[Xerostomia in the elderly: causes, consequences and treatment possibilities of dry mouth].

Xerostomia is in most cases caused by a decrease or discontinuity of salivation (hyposalivation). A physiological decrease in salivary gland function is not the main cause of hyposalivation. According to recent publications the general state of health plays a major role. Probably the most common cause is the use of medication with a salivary secretion inhibitory side effect. Proper patient assessment is essential to reveal the cause and to provide optimal treatment.

Aged↗
PubMed1994

Sedation for gastroscopy: a comparison between midazolam and midazolam with nalbuphine.

Forty patients received either midazolam or midazolam with nalbuphine in a double-blind randomised study of sedation for upper gastrointestinal endoscopy. There were less retching, gagging and salivation in the combination group compared to midazolam alone. They were also more cooperative. These resulted in greater ease of insertion of the gastroscope. There was no significant difference in the degree of amnesia in both groups. A significant decrease in oxygen saturation was noted in both groups during the procedure. Monitoring with a pulse oximeter is recommended when sedation is administered during gastroscopy.

Adolescent↗
PubMed1976

[On the cholinolytic activity of pramiverine].

Pharmacological experiments with the spasmolytic 4,4-diphenyl-N-isopropyl-cyclohexylamine hydrochloride (pramiverine, Sistalgin) are reported. The anticholinergic and spasmolytic action was tested in vitro on segments of abdominal organs in comparison with atropin, hyoscin-N-butylbromide and Eupaverin. Acetylcholine, arecoline, carbachol and pilocarpine were used as cholinergic agonists. Besides, neostigmine was applied. Pramiverine is distinguished by a strong anticholinergic and a papaverine-like spasmolytic component. In vitro the anticholinergic action of pramiverine on the small intestine (guinea pig, rabbit), gall bladder (guinea pig) and uterus (guinea pig, rat) was equally strong as the effect of atropine, but on the urinary bladder (guinea pig) the effect was 5 times weaker. The anticholinergic effect was also demonstrated in other models: intestinal spasms after neostigmine injection in the guinea pig; hypotensive effect after acetylcholine administration in rabbits, cats and dogs; salivation after pilocarpine administration in rabbits; tremorine test in rats. The gastric secretion in the Shay rat and the gastrointestinal passage were reduced or inhibited by pramiverine. The test substance was also active on oral application.

Animals↗
PubMed1994

Characterization of swallowing and defecation in Parkinson's disease.

UNLABELLED: Despite the high prevalence of Parkinson's disease, the pathophysiology of its gastrointestinal symptoms remains poorly understood. OBJECTIVES: to evaluate swallowing and defecatory function in patients with Parkinson's disease and age- and sex-matched controls and to correlate objective findings with subjective symptoms. METHODS: The following studies were performed on 13 patients with Parkinson's disease and seven controls: extrapyramidal function assessment, gastrointestinal symptom survey, videoesophagram, colon transit study, defecography, and anorectal manometry. RESULTS: Abnormal salivation (frequency, %, control vs. Parkinson's disease: 14 vs. 77, p < 0.05), dysphagia (14 vs. 77, p < 0.05), constipation (14 vs. 31, p < 0.05), and defecatory dysfunction (29 vs. 77, p < 0.05) were more common among Parkinsonian patients. However, videoesophagographic abnormalities were equally common in both groups. Colon transit time was significantly prolonged in the Parkinson's disease group. Altered puborectalis function was noted on defecography in 31% of Parkinson's disease subjects, but in none of the controls (p < 0.05). Anorectal manometry identified several abnormalities in the Parkinson's disease group, which included decreased basal anal sphincter pressures, prominent phasic fluctuations on squeeze, and a hyper-contractile external sphincter response to the rectosphincteric reflex. Many patients exhibited both slow transit and manometric abnormalities, and symptoms were poor predictors of test results. CONCLUSION: In this group of patients with mild to moderate Parkinson's disease, videoesophagographic abnormalities were not confined to the patients with Parkinson's disease. Studies of colonic and anorectal function, in contrast, identified a number of abnormalities. Therefore, colonic and anorectal dysfunction appears to be an early gastrointestinal manifestation of Parkinson's disease, and may represent the direct involvement of the gut by this disease process.

Aged↗
PubMed1996

Lithium toxicosis in a cow.

A case of lithium toxicosis is described in a cow that had consumed grease. Clinical signs included increased salivation, ataxia, reduced consciousness, seizures and diarrhea. No treatment was instituted. The grease did not contain high concentrations of other heavy metals or minerals.

Animals↗
PubMed1995

Comparison of the effects of desipramine on noradrenaline- and methoxamine-evoked venoconstriction in man.

1. The dorsal hand vein compliance technique was used to investigate the dual effect of tricyclic antidepressants at the noradrenergic synapse (i.e. noradrenaline uptake blockade leading to potentiation and alpha 1-adrenoceptor blockade leading to antagonism of the effect of noradrenaline). The effects of a single oral dose (100 mg) of desipramine (DMI) on venoconstrictor responses to locally infused noradrenaline and methoxamine, a selective alpha 1-adrenoceptor agonist with little affinity for the uptake mechanism, were examined. 2. Eight healthy male volunteers participated in four weekly experimental sessions. Each session was associated with one of the following treatment conditions: noradrenaline/DMI, noradrenaline/placebo, methoxamine/DMI, methoxamine/placebo. Subjects were allocated randomly to treatments and sessions according to a double-blind balanced design. Noradrenaline acid tartrate (0.33-33 ng min-1) and methoxamine hydrochloride (0.0135-135 micrograms min-1) were infused into the superficial dorsal hand vein; each dose was infused for 5-7 min with 5 min intervening washout periods. Systolic and diastolic blood pressure and pulse rate were recorded before the infusion and immediately after the infusion of the highest dose. Salivation, an index of anticholinergic activity of the antidepressant, was measured by the dental roll technique. 3. Both noradrenaline and methoxamine produced dose-dependent venoconstriction: the geometric mean ED50 for noradrenaline was 4.41 ng min-1 and for methoxamine was 2558 ng min-1; the potency ratio (noradrenaline/methoxamine) was 2884. DMI shifted the dose-response curve for noradrenaline to the left (ANOVA: P < 0.025), resulting in a dose-ratio of 0.26. DMI did not affect the dose-response curve for methoxamine significantly; the dose ratio was 1.24. 4. None of the local infusions and/or systemic treatments had any significant effects on supine systolic and diastolic blood pressure and pulse rate. 5. DMI caused a substantial (47.6%) reduction in salivary output that significantly differed from the slight statistically insignificant increase (5.8%) of salivary output recorded after placebo. 6. These results show that a single oral dose (100 mg) of DMI causes significant potentiation of the response to noradrenaline without significantly affecting the response to methoxamine. The potentiation is likely to be due to uptake blockade since the response to methoxamine was not affected. Furthermore, the lack of significant antagonism of the response to methoxamine indicates that a single oral dose (100 mg) of DMI does not cause sufficient alpha 1-adrenoceptor blockade to be detected as a pharmacodynamic change in our test system.

Adolescent↗
PubMed1996

Effect of the novel high affinity choline uptake enhancer 2-(2-oxopyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofuro[2,3-b] quinolin-4-yl)acetoamide on deficits of water maze learning in rats.

The pharmacological properties of MKC-231 (2-(2-oxopyrrolidin-1-yl)-N- (2,3-dimethyl-5,6,7,8-tetrahydrofuro[2,3-b]quinolin-4-yl) acetoamide, CAS 135463-81-9) in comparison with an acetylcholinesterase (AChE) inhibitor, tacrine (CAS 1684-40-8) were studied. MKC-231(10(-10)-10(-6) moll) significantly increased high affinity choline uptake (HACU) when it was incubated with the hippocampal synaptosomes of ethylcholine mustard aziridinium ion (AF64A) treated rats, but not of normal rats. MKC-231 did not affect the AChE activity, [3H]- quinuclidinyl benzilate binding, and [3H]-pirenzepine binding. Oral administration of MKC-231 (1-10 mg/kg) significantly improved the learning deficits in the Morris' water maze of AF64A-treated rats, but it did not produce any significant side effects, like tremor, salivation or hypothermia, which were observed in rats treated with high doses of tacrine. Tacrine (0.1-3 mg/kg p.o.) failed to ameliorate the learning deficits in AF64A-treated rats. These results suggest that MKC-231 is a novel and quite unique compound, which improves the memory impairment induced by AF64A through the enhancement of HACU without any side effects at the effective doses.

Acetylcholinesterase↗
PubMed1996

Acute poisoning with Diffenbachia picta.

Plants from the Araceae family contain unidentified volatile compounds that are highly irritative or corrosive. Patient aged 38 was admitted with acute poisoning with Diffenbachia picta exhibited as severe salivation, burning and pain of the oral cavity, mucosal edema and blistering. Treatment was conservative similar to that in corrosive poisonings. Patient was discharged after 14 d hospitalization without postburning complications.

Administration, Topical↗
PubMed1996

Clinical perspectives of intravenous ketamine anaesthesia in peafowl (Pavo cristatus).

A total of 29 peafowl (Pavo cristatus), rectified surgically for infraorbital abscesses (n = 22), lacerated wounds (n = 4), and fractures of tibia (n = 2) and radius (n = 1), were anaesthetized by the intravenous administration of ketamine hydrochloride (Inj. Calypsol, Gedeon Richter, Hungary) in a dose of 15 20 mg/kg body weight. Divided doses (10 mg + 5 mg + 5 mg) were used with an interval of 1-2 min. No premedication was undertaken in any of the birds. Anaesthesia lasted for about 15 min and the birds gained their feet completely after 30 min to 3 hours. The respiration rate was markedly depressed (8-10/min) and the respiratory pattern was deep abdominal. Only a slight increase was observed in the heart rate. Analgesia was incomplete and muscle relaxation was not satisfactory. Mild salivation was also noticed in some of the birds (n = 3). Recovery, although not smooth, was uneventful.

Abscess↗
PubMed1997

Reproductive toxicity studies of D-camphor in rats and rabbits.

The embryotoxicity of D-Camphor (CAS 76-22-2), orally employed for the treatment of hypotonic circulatory dysregulations, was investigated in rats and rabbits. D-Camphor elicited no evidence of teratogenicity when administered orally during the fetal period of organogenesis to pregnant rats at doses up to 1000 mg/kg b.w./day, and to pregnant rabbits at doses up to 681 mg/kg b.w./day. The no-observed-effect level for the fetal organism for the rat was above 1000 mg/kg b.w., and for the rabbit above 681 mg/kg b.w. In rat dams a dose-dependent reduction in food intake and salivation was noted from 464 mg/kg b.w./p.o. onwards. The high dose of 1000 mg/kg b.w./d p.o. resulted in fairly pronounced signs of toxicity such as clonic convulsion, pilo-erection, reduced motility and reduced body weight gain. In rabbit dams the high dose level of 681 mg/kg b.w./d p.o. resulted in reduced body weight gain and food consumption. No increased incidence in variations, retardations or malformations were observed at any of the treated dose levels not even at the highest tested dose level (rat: 1000 mg/kg b.w./d p.o.; rabbit: 681 mg/kg b.w./d p.o.). The daily maximum human therapeutic camphor dose is approximately 1.43 mg/kg b.w. Hence, under the present test conditions the therapeutic ratio is above 450 for the endpoint embryotoxicity reflecting a wide margin of safety.

Animals↗
PubMed1997

New 5-aminoacyl-5,10-dihydro-11H-dibenzo[b,e][1,4]diazepin-11-ones with antiarrhythmic activity.

A series of new 5-substituted tricyclic 5,10-dihydro-11H-dibenzo[b,e][1,4]-diazepin-11-ones was identified as potential antiarrhythmic agents against bradyarrhythmias [1, 2]. The in vitro and in vivo interactions of the compounds with muscarinic receptors and the antiarrhythmic activity were examined. In receptor binding studies some derivatives showed a high affinity to the cardiac M2 receptor (Ki 10 nmol/l), an equal or smaller affinity to cortical M1 receptor and a lower affinity to the glandular M3 binding site. Functional experiments showed the derivatives as competitive antagonists with high affinity to the cardiac and smaller affinity to the intestinal muscarinic receptor. In vivo experiments correspond with the M2 selectivity. First the vagal or agonist-induced bradycardia was inhibited in rats and guinea pigs while the McNA-343 induced increase of blood pressure, methacholine-induced bronchi and bladder constriction as well as the salivation were inhibited only at higher doses. In conscious cats the tachycardia was examined in comparison with pupillomotoricity. The effect duration and the therapeutical range were determined in comparison to the M2 selective blocking agent AF-DX116. The antiarrhythmic activity was examined compared to quinidine sulfate in CaCl2-arrhythmia of rats, in atrial fibrillation and atrial flutter in dogs according to Scherf [2] and in electric induced atrial fibrillation under vagal stimulation in cats. In the atrial arrhythmias the derivatives are clearly longer effective than quinidine sulfate. The antiischemic activity was examined in the two-stages coronary ligature in dogs according to Harris. The long-running regularization of ectopies (about 2 h after i.v. injection) occurred without decrease of the heart rate, an effect particularly convenient to therapy of bradycardic dysrhythmias.

Animals↗