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PubMed1980

The peripheral anticholinergic activity of tricyclic antidepressants: comparison of amitriptyline and desipramine in human volunteers.

The effects of three single oral doses (25 mg, 50 mg and 100 mg) of amitriptyline and desipramine, and of placebo, were compared on a range of cholinergic functions (resting pupil diameter, pilocarpine-evoked miosis, baseline-sweating, carbachol-evoked sweating, salivation, heart rate) in eight healthy volunteers. Three measures (pilocarpine-evoked miosis, carbachol-evoked sweating and salivation) reflected the antimuscarinic property of the antidepressants; in two tests (pilocarpine-evoked miosis and salivation) amitriptyline appeared to be more potent than desipramine. Resting pupil diameter was not affected by amitriptyline, whereas desipramine caused mydriasis, indicating that pupil size is not a reliable measure of anticholinergic activity in the case of drugs which also affect adrenergic mechanisms. Baseline-sweating and heart rate were not affected by the antidepressants.

Adult↗
PubMed1977

[Effects of a new minor tranquilizer, 10-chloro-3-methyl-1 1b-(2-chlorophenyl)-2,3,5,6,7,11b-hexahydrobenzo [6,7]-1,4-diazepino [5,4-b]-oxazol-6-one (CS-386), on the after-discharge and behavior induced by electrical stimulation of the amygdala in freely-moving cats (author's transl)].

Effects of a new minor tranquilizer, CS-386, on the after-discharge(AD) and behavior induced by amygdaloid electrical stimulation in freely-moving cats were compared with those of cloxazolam, oxazolam, diazepam, chlordiazepoxide, phenobarbital and chlorphromazine. Effects on change of the AD threshold and duration and on facial twitching, salivation and tonic-clonic convulsion were investigated. CS-386, cloxazolam and oxazolam inhibited amygdaloid AD. CS-386 had the most potent inhibitory effect. These drugs depressed all behavior described above. Diazepam had no effects on the AD threshold, but decreased the AD duration and inhibited the behavior. Chlordiazepoxide had no apparent effects on amygdaloid AD and on facial twitching. Salivation was inhibited with high doses of administration. Phenobarbital shortened the AD duration and at a high dose elevated the AD threshold. This drug also inhibited salivation, but inhibitory effects on other behavior required doses as high as 90 mg/kg. These results suggest that CS-386, cloxazolam and oxazolam are compounds belonging to a classification different from that of chlorpromazine. CS-386 in particular, is a more potent drug chlordiazepoxide, diazepam and phenobarbital and acts on the amygdala itself.

Administration, Oral↗
PubMed1987

Effects of dopamine on the secretion of glycoproteins from the functional segments of the rat submandibular gland.

The action of dopamine (DA) on salivation and the secretion of marker glycoproteins (GP) from secretory cells of the rat submandibular gland (SMG) was investigated using various blockers at doses of 1 or 2 mg/kg (i.v.). DA at doses from 5 to 40 mg/kg (i.p.) dose-dependently increased salivation and the concentration of protein in SMG saliva. The order of inhibitory potency on salivation was propranolol (PPR) greater than phentolamine (PHN) much greater than haloperidol (HAL) when DA was administered i.p. at a dose of 10 mg/kg and PHN much greater than HAL much greater than PPR when the dose of DA was 40 mg/kg. The concentration of protein in saliva after pretreatment with HAL or PHN increased significantly at a dose of 40 mg/kg of DA, but did not increase at a dose of 10 mg/kg of DA. Moreover, pretreatment with PPR decreased it at both doses of DA. The electrophoretic profiles of GP in DA-evoked saliva showed two characteristic main bands of GP I (130 KDa) and GP IV (21.5 KDa) contained in the acinar cells (AC) and a minor band of GP III (31 KDa) which originated from the granular tubular cells (GT). The profile was not changed by pretreatment with PHN and HAL when DA was administered at a dose of 10 mg/kg, but at a dose of 40 mg/kg, the intensity of band I increased. Pretreatment with PPR, when DA was administered at 40 mg/kg, caused an increase in the intensity of band III and a reduction in that of band I. These results suggest that DA, at low doses, affects the AC, whereas at a higher dose, it affects both the AC and GT.

Animals↗
PubMed2002

Effect of pilocarpine mouthwash on salivary flow.

Pilocarpine is a cholinergic agonist that increases salivary flow and has been used to treat xerostomia. Oral intake is the most frequent route of administration. Adverse effects are dose-dependent and include sudoresis, facial blushing and increased urinary frequency. The objective of the present study was to evaluate the effects of topical pilocarpine solutions as mouthwashes on salivary flow and their adverse effects on healthy subjects. Forty volunteers received 10 ml 0.5, 1 and 2% pilocarpine solutions or 0.9% saline in a randomized, double-blind, placebo-controlled manner. Salivation was measured before and 45, 60 and 75 min after mouth rinsing for 1 min with 10 ml of saline or pilocarpine solutions. Vital signs were measured and ocular, gastrointestinal and cardiovascular symptoms, anxiety and flushing were estimated using visual analog scales. There was a dose-dependent increase in salivation. Salivation measured after 1 and 2% pilocarpine (1.4 +/- 0.36 and 2.22 +/- 0.42 g, respectively) was significantly (P<0.001) higher than before (0.70 +/- 0.15 and 0.64 +/- 0.1 g), with a plateau between 45 and 75 min. Cardiovascular, visual, gastrointestinal and behavioral symptoms and signs were not changed by topical pilocarpine. Mouth rinsing with pilocarpine solutions at concentrations of 1 to 2% induced a significant objective and subjective dose-dependent increase in salivary flow, similar to the results reported by others studying the effect of oral 5 mg pilocarpine. The present study revealed the efficacy of pilocarpine mouthwash solutions in increasing salivary flow in healthy volunteers, with no adverse effects. Additional studies on patients with xerostomia are needed.

Adolescent↗
PubMed1978

Effects of a stimulant drug on extraversion level in hyperactive children.

7 hyperactive children in a pilot study, and 15 hyperactive and 15 non-hyperactive control children in a later study, were assessed for salivation to lemon juice stimulation, reactive inhibition on an audio-vigilance task, and visual-motor maze errors. Hyperactive children were tested under stimulant drug and nondrug conditions and nonhyperactive children twice under nondrug conditions. Pilot study hyperactive children displayed significantly fewer maze errors and somewhat greater salivation and lesser reactive inhibition levels under the drug than the nondrug conditions. Follow-up study control children did not differ significantly between test occasions on any measure, while the hyperactive children displayed significantly fewer maze errors, more salivation, and less reactive inhibition under the stimulant drug, indicating significant decreases in extraversion after the stimulant drug.

Adolescent↗
PubMedDate not supplied

Pilocarpine-induced salivary secretion, kinin system and nitric oxide in rats.

In anaesthetized rats, intraperitoneal injection of pilocarpine (0.1 to 1 mg.Kg-1) induced a dose-dependent flow of saliva. During salivation by pilocarpine (0.5 mg.Kg-1), the blood content of submaxillary glands was not significantly increased but the blood volume of the animals was reduced. The salivary flow rate induced by pilocarpine was similar in normal and kininogen-deficient rats. L-NG-nitro-arginine (L-NOARG, 35 mg.Kg-1), a nitric oxide synthesis inhibitor, increased the salivary flow elicited by pilocarpine (0.5 mg.Kg-1). L-NOARG did not modify the blood volume loss but decreased the blood content of the submaxillary glands. The volume of salivary secretion induced by isoproterenol (250 mg.Kg-1) was lower in kininogen-deficient rats than in normal rats. It was significantly reduced by HOE 140 (2 mg.Kg-1), a bradykinin antagonist. L-NOARG increased the salivary flow induced by isoproterenol during the ten first minutes of collection but suppressed it thereafter. We concluded that kinins are not involved in the stimulating effect of pilocarpine on rat salivary glands but these peptides would participate to the development of the salivation induced by isoproterenol in rats. Nitric oxide contributes to the control of the vascular tone in rat salivary glands. The influence of L-NOARG on salivation would be explained by its effects on blood pressure and vascular resistances.

Amino Acid Oxidoreductases↗
PubMed1989

Cortically evoked responses of superior salivary nucleus neurons in the cat.

Salivation can be controlled by the inputs from the cerebral cortex as well as from the sensory nerves. However, there has been no detailed report so far on the inputs to superior salivatory nucleus (SSN) neurons from the cerebral cortex. The responses of SSN neurons to electrical stimulation of orbital and coronal gyri were investigated in ketamine anesthetized cats. A total of 56 SSN neurons were identified by the antidromic spike responses to stimulation of the right chorda tympani nerve. Their responsiveness to stimulation of the orbital and anterior coronal gyri and the lingual nerve at the ipsilateral side was tested. Thirty-five neurons (63%) responded with spikes to stimulation of the orbital and/or coronal gyri. They were also activated by stimulation of the lingual nerve. Other eleven neurons (20%) received the inputs from the lingual nerve only. The remaining 10 neurons (17%) failed to respond to stimulation of either the cerebral cortex or the lingual nerve. The mean latencies of the responses to stimulation of the orbital gyrus, coronal gyrus and lingual nerve were 29.0 ms (n = 28), 22.7 ms (n = 33) and 10.2 ms (n = 46), respectively. In this study, the excitatory inputs converging from the cerebral cortex and the lingual nerve, found in 63% of SSN neurons, could play an important role in submandibular and sublingual salivation. Cortically induced salivation, in particular, may be involved in salivary secretion in the conditioned reflexes as well as in mastication.

Animals↗
PubMed1986

Dualism in the effect of cholinolytics upon the human parotid gland deprived of parasympathetic control.

Dualism in the effects of atropine, and metixene upon the denervated human parotid salivary gland is demonstrated by the fact that they suppress pilocarpine secretion while themselves causing an extremely intense and prolonged salivation. A still stronger cholinolytic, chlorosyle, although causing salivation, blocks paradoxical salivation initiated by atropine and metacine. With respect to the latter ligands, chlorosyle acts as a partial agonist. Dualism in the cholinolytics' effect is conditioned by generation, following chronic enervation of the gland, of cholinoreceptor subpopulations of different functional significance and evolutional maturity. Depending on the length of the cholinoreceptor reactive zone, cholinolytics initiate blockade of some receptors and excitement of others.

Atropine↗
PubMed1994

Interrelationship between esophageal challenge with mechanical and chemical stimuli and salivary protective mechanisms.

Using our newly developed model of esophageal perfusion in humans, we were able to study the esophagosalivary reflex in 20 healthy volunteers (12M, 8F; mean age 40 yr). The placement of the intraesophageal catheter resulted in a 6.3-fold increase in the salivation rate over the baseline value (2.27 +/- 0.28 vs. 0.36 +/- 0.06 ml/min; p = 0.02), whereas inflation of the catheter balloons evoked a 6.9-fold increase (2.52 +/- 0.21; p < 0.001) in the rate of salivation. A stepwise and significant decline of salivation (p = 0.02), observed during subsequent perfusion with NaCl was prevented when perfusion with HCl and HCl/pepsin solutions was implemented. The placement of the intraesophageal catheter resulted in a significant increase of salivary pH over its basal value (7.77 +/- 0.05 vs. 6.89 +/- 0.11; p < 0.001). A gradual decline of salivary pH during subsequent perfusion with NaCl was eliminated when saline was replaced with HCl or HCl/pepsin (7.76 +/- 0.04 vs. 7.46 +/- 0.09; p < 0.01). Intraesophageal tubing enormously potentiated the viscosity of saliva (44.50 +/- 9.0 vs. 9.3 +/- 1.0 mPa.s; p < 0.001). A subsequent decline of viscosity during continuous perfusion with saline was also prevented when HCl was substituted for NaCl (29.95 +/- 4.5 vs. 19.50 +/- 3.30; p < 0.05). A significant potentiation of salivary volume, viscosity, and pH during esophageal stimulation of mechano- and chemoreceptors may suggest a contributing role of the esophagosalivary reflex in the maintenance of the esophageal mucosal integrity under the impact gastroesophageal reflux.

Adult↗
PubMed1996

The effects of a long-term powdered diet on the amounts of two principal neurotransmitters in the major salivary glands and on stimulated salivary secretion in mice.

The amounts of 2 principal neurotransmitters, acetylcholine (ACh) and norepinephrine (NE) in the 3 major salivary glands, and pilocarpine-, isoproterenol- and phenylephrine-induced salivation in male mice fed a powdered diet for 16 weeks were compared with those in mice fed a standard pellet diet (as control). There were no significant differences in the final body weights of mice fed the powdered diet and the control diet. The only salivary gland in the powdered diet fed mice to increase significantly in weight was the sublingual gland. Mice fed the powdered diet had significantly increased ACh concentrations and contents, but had decreased amounts of NE, in the submandibular and sublingual, but not the parotid glands. The salivation stimulated by pilocarpine was markedly decreased in mice fed the powdered diet, whereas the salivation stimulated by phenylephrine or isoproterenol was not. These findings indicate that reduced mastication affects not only the secretory function but also the amounts of these neurotransmitters in the salivary glands of mice.

Acetylcholine↗
PubMed1993

Gastrointestinal symptoms in Parkinson disease: 18-month follow-up study.

In a recent study we identified abnormal salivation, dysphagia, nausea, constipation, and defecatory dysfunction as those gastrointestinal (GI) symptoms associated with Parkinson disease (PD) and characterized their relationship to PD severity and therapy. In this study, we re-evaluated these symptoms and their relationship to parameters of PD 18 months later. Sixty-six percent of the original participants responded. Over the 18 months, 68% of originally untreated PD subjects commenced anti-PD therapy. Abnormal salivation, dysphagia, nausea, constipation, and defecatory dysfunction were again identified as those GI symptoms more common in PD. Constipation increased both in severity and frequency. Comparison of GI symptom scores and parameters of PD dysfunction failed to reveal significant progression of either GI symptomatology or PD dysfunction, or the development of new GI symptoms over the 18-month period. This study validates our GI dysfunction assessment system and confirms abnormal salivation, dysphagia, nausea, constipation, and defecatory function as those GI symptoms truly associated with PD. A direct relationship between PD and its related GI symptoms is again supported.

Aged↗
PubMed1996

[Anxiolysis, sedation, and stress reduction following oral premedication with midazolam in adults. A comparison with dipotassium clorazepate and placebo].

Benzodiazepines are the most commonly used anxiolytic agents. Among the benzodiazepines, midazolam has the advantage of a short elimination half-life, which is especially useful in outpatient surgery. However, in contrast to other commonly prescribed benzodiazepines, such as chlorazepate dipotassium, oral premedication with midazolam has not been thoroughly investigated. Therefore, the present study was performed to compare anxiolysis, sedation and stress reduction with midazolam and clorazepate dipotassium in adults. METHODS. After IRB approval and informed consent had been obtained, 85 patients scheduled for breast biopsy were studied. The patients were chosen at random to receive either 7.5 mg midazolam (n = 29), 20 mg clorazepate dipotassium (n = 28) or placebo (n = 28) preoperatively. Before premedication, immediately prior to surgery and postoperatively in the recovery room, the following parameters were determined with visual analogue scales (VAS): "asthenia," "depression," oral salivation, muscle tension, motoric restlessness and sweating of the palms. In addition, anxiety (STAI-G-X-1, Spielberger), heart rate and arterial blood pressure were measured. Before patients underwent surgery, the degree of sedation was evaluated by the anaesthesiologist. RESULTS. Clorazepate dipotassium and midazolam both caused a reduction in anxiety as compared with the placebo (P < 0.05). Only clorazepate dipotassium reduced anxiety postoperatively (P < 0.05). Neither midazolam nor clorazepate dipotassium caused a reduction in "asthenia" and "depression." Midazolam was more effective in preventing increased blood pressure than clorazepate dipotassium and the placebo (P < 0.05). Furthermore, after premedication with midazolam, salivation, muscle tension, motoric restlessness and sweating of the palms remained stable, in contrast to the results after premedication using clorazepate dipotassium or placebo (P < 0.05). CONCLUSIONS. The anxiolytic effects of 7.5 mg midazolam and 20 mg clorazepate dipotassium were similar after oral application. However, the anxiolytic effect of midazolam is shorter-lived than that of clorazepate dipotassium. In contrast to clorazepate dipotassium, midazolam produced no increase in arterial blood pressure and stabilized oral salivation, production in the palms, muscle tension and motoric restlessness.

Adult↗
PubMed1988

Antihypertensive effects of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) in conscious dogs.

Low doses of 8-OH-DPAT (10 and 25 micrograms/kg) administered subcutaneously (s.c.) to renal hypertensive mongrel dogs caused decreases in systolic blood pressure which persisted for 3 h. Mild salivation and hyperventilation were observed with both doses. A short-lasting (less than 60 min) depressor response was seen with 100 micrograms/kg s.c. Prominent hyperventilation and salivation accompanied this response. A still higher dose (250 micrograms/kg s.c.) induced tremor, signs of anxiety and occasional vomiting in addition to the hyperventilation and salivation. Paradoxically, no cardiovascular activity was noted at this dose.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1988

Preventive action of quisqualic acid against grayanotoxin-induced suppression of locomotor activity in mice.

Grayanotoxin-III (GTX-III) is a constituent in leaves of Pieris japonica D. Don which exhibits, in vitro, the ability to open voltage-sensitive sodium channels in various excitable tissues. Effects of systemic administration of GTX-III were studied in vivo using Std-ddy mice. Salivation, vomiting and paralysis of the hind paws invariably occurred in mice injected intraperitoneally with 0.1 or 0.25 mg/kg of GTX-III. The writhing response to an intraperitoneal injection of acetic acid was considerably diminished by pretreatment of animals with the toxin. The grayanoid also caused a profound attenuation of the response to caudal compression, while inducing no significant alteration of that to thermal injury. Pretreatment with GTX-III resulted in a significant decrement of the time required for loss of the righting reflex induced by pentobarbital, with a concomitant delay in recovery. Mice injected with the toxin exhibited a significant and restorable suppression of coordination, and a long-lasting suppression of spontaneous locomotor activity in both horizontal and vertical directions. Neither tetrodotoxin (1-5 micrograms/kg, i.p.) nor Ro15-1788 (1-5 mg/kg, i.p.) prevented the GTX-III-induced suppression of locomotion. Atropine (5-10 mg/kg, i.p.) failed to antagonize the GTX-III-induced suppression but protected against salivation induced by the toxin without affecting other symptoms. Intracerebroventricular injection of quisqualic acid (0.5 microgram), one of the agonists for central glutamate receptors, but not that of tetrodotoxin (5 ng) prevented the GTX-III-induced suppression of horizontal movement. These results suggest that GTX-III may elicit its depressant action on horizontal locomotion possibly through interacting with central glutamatergic neurons rather than activating voltage-sensitive sodium channels in the brain. Possible involvement of muscarinic cholinergic neurons in the GTX-III-induced salivation is also suggested.

Analgesics↗
PubMed1987

Dopaminergic and alpha 1-adrenergic properties of B-HT920 revealed in morphine-dependent rats.

B-HT920 is known to be a selective alpha 2-adrenoceptor agonist, and has been used in a study on morphine-withdrawal in rats. In accordance with other alpha 2-agonists B-HT920 was found to potentiate "jumping" and to reduce "body shakes." However, B-HT920 did not suppress body weight loss. Furthermore, it induced strong salivation and prevented ptosis (described for the alpha 1-adrenergic agonist ST-587). Rearing and locomotor activity appeared to be enhanced, an effect shared by dopamine-agonist lisurid. The effects of B-HT920 have been specified using the alpha-adrenergic antagonists yohimbine and prazosin and the dopamine antagonist haloperidol. Yohimbine could not antagonize any of the actions of B-HT920. However the increase in rearing and locomotion was blocked by haloperidol. The induction of salivation was prevented by prazosin. Pretreatment with prazosin showed a decrease in the loss of body weight caused by B-HT920, while pretreatment with yohimbine showed that B-HT920 induced an increased loss in body weight. These data suggest that B-HT920 under certain conditions exerts dopamine-agonistic actions in stimulating locomotor activity and alpha 1-adrenergic actions in inducing salivation and enhanced loss of body weight.

Adrenergic alpha-Agonists↗
PubMed1996

Effect of PG-SPI and PG-KII, two novel and natural tachykinins, on salivary secretion in the rat.

In an in vivo study of salivation in rats, the scialogogic effects of two natural and amphibian tachykinins, PG-SPI and PG-KII, which activate distinct tachykinin receptors, were compared with those of the tachykinins substance P, neurokinin A and B, and kassinin. The rank order of potencies of these peptides injected intravenously on salivation was: PG-SPI = SP > or = PG-KII = KASS > NKA > > NKB. Atropine (1 mg/kg. i.v.) had no effect on PG-SPI-, SP-, and NKA-induced salivation, but reduced that stimulated by PG-KII and KASS. We conclude that PG-SPI and PG-KII increase salivary secretion through different mechanisms and that rat salivary glands contain PG-SPI-and PG-KII-sensitive receptors.

Amino Acid Sequence↗
PubMed1998

Effects of tizanidine administration on precipitated opioid withdrawal signs in rats.

An opioid withdrawal syndrome was precipitated by naloxone administration in rats treated with morphine. The withdrawal caused alteration of several physiological signs. The aim of the study was to investigate whether the altered physiological profiles were modified by utilising tizanidine, an alpha 2 adrenergic receptor agonist which is capable of affecting faecal and urinary excretion, rectal temperature, pain threshold levels and salivation. To induce an opioid withdrawal syndrome, morphine was administered in three daily intraperitoneal injections for four days at doses of 9, 16 and 25 mg/kg (1st day), 25, 25 and 50 mg/kg (2nd day), 50, 50 and 50 mg/kg (3rd day) and 50, 50 and 100 mg/kg (4th day): naloxone was injected (30 mg/kg) i.p. 180 min after the last morphine injection. Tizanidine was administered orally at 0.17, 0.35 and 0.7 mg/kg, 60 min after the last morphine injection. Signs such as faecal and urine excretion, rectal temperature and latency times to thermal stimulus, salivation, jumping and wet dog shakes were affected in different ways by morphine, naloxone, tizanidine and by the combination of these agents. Notably, the administration of tizanidine in rats receiving morphine and naloxone decreased the intensity of certain withdrawal symptoms, including altered excretion of faeces and urine, salivation and wet dog shake behavior. Body temperature levels and nociceptive threshold values were also modified. The effects caused by tizanidine administration may be due to its alpha 2 receptor agonist activity interfering with a mechanism involved in the regulation of these previously mentioned withdrawal symptoms. Thus, the use of this drug may be indicated as a possible control of the acute phase of opioid withdrawal in heroin addicts.

Adrenergic alpha-Agonists↗
PubMed1996

[Evaluation of vectorial capacity of Glossina tachinoides (Diptera, Glossinidae) infected by Trypanosoma (Nannomonas) congolense: epidemiological implications].

A total of 182 Glossina tachinoides were infected with Trypanosoma congolense savannah type. Infection rates were determined according to microscopical examination of dissected flies and PCR on proboscis. Different techniques of trypanosomes detection in the saliva of live tsetse flies were compared. Results show a high percentage of immature infection rates. PCR amplification of trypanosomes in tsetse flies proboscis confirm parasitological observations. The salivation technique showed fluctuations of the number of trypanosomes deposited with saliva. Variability between individual flies was observed in the mean number of parasites ejected, the rate of positive salivates detected by PCR and the rate of infected mice. PCR technique was as efficient as parasitological technique to detect trypanosomes in the salivates. The infectivity on mice was the less efficient method. These results improve our knowledge on G. tachinoides vectorial competence in the laboratory, and precise the role of this tsetse species in the epidemiology of this disease.

Africa South of the Sahara↗