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PubMed1989

Muscarinic actions and receptor binding of the enantiomers of BM 130, an alkylating analog of oxotremorine.

The enantiomers of the oxotremorine analog N-[4-(2-chloromethylpyrrolidine)-2-butynyl]-2-pyrrolidone (BM 130) were synthesized. The LD50 values of (+)- and (-)-BM 130 in mice (i.v.) were 10.4 +/- 1.4 and 13.5 +/- 1.9 mumol/kg, respectively. Atropine and N-methylatropine poorly protected against the lethal effects, suggesting that they were nonmuscarinic in nature. When administered i.v. to mice, (+)- and (-)-BM 130 were equipotent in producing peripheral and central muscarinic effects. ED50 values were 1.3 to 1.4, 2.8 to 3.2 and 0.20 to 0.26 mumol/kg, respectively, for salivation, tremor and analgesia (tail-flick assay). After i.p. injection, tremor was not observed and analgesic potency was reduced more than 10-fold compared to the i.v. route. The aziridinium ions [(+)- and (-)-BM 130A], formed by spontaneous cyclization of (+)- and (-)-BM 130, were virtually equipotent in eliciting contractions of the isolated guinea pig ileum and in causing salivation in mice. Their LD50 values in mice (i.v.) were 1.1 +/- 0.2 and 2.1 +/- 0.3 mumol/kg, respectively. The enantiomers of BM 130A had similar affinity for muscarinic receptors in the rat cerebral cortex as measured by competitive inhibition of (-)-[3H]N-methylscopolamine binding at 0 degrees C. The rate constants for alkylation of muscarinic receptors, obtained at 37 degrees C by measuring the decline in (-)-[3H]-3-quinuclidinyl benzilate binding to cortical homogenates that had been treated with various concentrations of (+)- and (-)-BM 130A for 20, 45 or 90 min, differed significantly for the two enantiomers.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkylation↗

PubMedDate not supplied

[The hemodynamics of the parotid glands in children consuming carbohydrates].

The rate of sweets consumption was shown to determine, to a large extent, the salivary glands function. In children rarely consuming sweets the parotid blood flow and salivation increased after intake of a 10% sucrose solution. In children abusing sweets even crystal sugar failed to change the parotid glands blood filling with salivation virtually unaltered.

Candy↗

PubMed1988

Deprenyl antagonizes acute lethality of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice.

In Charles River CFW mice, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) caused lethality with an LD50 of 53.8 mg/kg s.c. In mice pretreated with deprenyl, no lethality occurred with MPTP doses up to 110 mg/kg s.c. MPTP alone at doses of 30 to 90 mg/kg s.c. caused marked salivation, licking and grooming, hyperlocomotion, hyperreactivity and convulsions during the 1st hr, followed by depression, continued salivation and respiratory distress at 2 to 3 hr and at longer times, with death occurring at the higher doses. In deprenyl-pretreated mice, MPTP produced only mild and transient effects. 1-Methyl-4-phenylpyridinium (MPP+) was more potent in causing lethality than was MPTP, and deprenyl did not affect its lethality. MPTP lethality was not antagonized by EXP 561 [4-phenyl-bicyclo-(2,2,2)octan-1-amine hydrochloride monohydrate], an uptake inhibitor that prevented the neurotoxic effects of a lower dose of MPTP on striatal dopamine and cortical norepinephrine neurons. In addition to deprenyl, other monoamine oxidase (MAO) inhibitors effective in inhibiting MAO-B (MD 240928 (R-3-[4-((3-chlorophenyl)methoxy)phenyl]-5-[(methylamino)methyl]-2- oxazolidinone methanesulfonate) and pargyline) protected against MPTP-induced lethality, but LY 51641 (N-[2-(o-chlorophenoxy)ethyl]cyclopropylamine hydrochloride) (a selective inhibitor of MAO-A) did not. The protective effect of deprenyl against MPTP-induced lethality was dose-dependent over a dose range of 0.01 to 10 mg/kg; in this range deprenyl inhibited MAO type B (MAO-B) in brain and liver. A 10-mg/kg i.p. dose of deprenyl antagonized MPTP-induced lethality as long as 14 days.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1988

Reproductive studies of NY-198 in rats. I. Fertility study.

Lomefloxacin (NY-198), a new antibacterial agent, was administered daily by gavage to groups of 22 male and 22 female rats at dosages of 30, 100 or 300 mg/kg/day. Males were dosed for 71 days before pairing and then until termination, and females were dosed for 15 days before pairing, throughout mating and until Day 7 of gestation. Females were killed on Day 20 of gestation for examination of their uterine contents. Males were killed after approximately 14 weeks treatment and their reproductive organs were weighed and retained. At 300 mg/kg/day the majority of animals showed increased salivation, water intake was slightly increased throughout the treatment period in males and before pairing in females whereas food intake showed a slight, transient reduction during the first few days of treatment in both sexes. Body weight gain of males was marginally depressed during the first week of treatment, but no other signs of reaction to treatment were observed. At 30 and 100 mg/kg/day some animals exhibited increased salivation after being dosed. At all dosages, NY-198 was without adverse effects upon mating performance and fertility, or upon survival, growth and development in utero. On the basis of the above results it is considered that the no effect level with respect to reproduction and breeding performance of treated F0 animals and the in utero development of the foetuses was 300 mg/kg/day. A dosage of 100 mg/kg/day was considered to be the no effect level for somatic changes in the F0 animals, and even at the highest dosage of 300 mg/kg/day only slight effects were recorded on the F0 animals.

4-Quinolones↗

PubMed1987

Muscarinic actions of an N-methyl-N-2-bromoethylamino analog of oxotremorine (BR 401) in the mouse.

The pharmacological effects of N-[4-(2-bromoethylmethylamino)-2-butynyl]-2-pyrrolidone (BR 401) were compared in the mouse with those of N-[4-(2-chloroethylmethylamino)-2-butynl]-2-pyrrolidone (BM 123) and oxotremorine. BR 401 was more toxic than oxotremorine and BM 123 when administered i.v. (LD50, 0.7 mumol kg-1), but less toxic than oxotremorine when given i.p. (LD50, 39 mumol kg-1). Atropine and methylatropine (10 mumol kg-1 i.p.) increased the LD50 value of BR 401, given i.v., 75- to 100-fold. Upon i.v. administration, BR 401 was 2- to 3-fold more potent than oxotremorine and 10 to 20 times more potent than BM 123 in producing central (tremor and analgesia) and peripheral (salivation) muscarinic effects. However, after i.p. administration BR 401 was 3-fold less potent than oxotremorine in eliciting tremor and analgesia. The aziridinium ion (BR 401A), formed by cyclization of BR 401, produced salivation but no tremor. These observations suggest that BR 401 when given i.v. penetrates effectively into the central nervous system where it cyclizes rapidly to the pharmacologically active aziridinium ion. In contrast, after i.p. administration a large proportion of BR 401 will cyclize before it can reach the central nervous system. BM 123, because of its slower cyclization, enters the central nervous system effectively also by the i.p. route. Thus, central potency of 2-haloethylamines such as BR 401 and BM 123 is critically dependent not only on the rate of cyclization, but also on the route of administration. The duration of tremor induced by BR 401 and BM 123 was considerably shorter than that induced by oxotremorine.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗

PubMed1985

Comparison of paradoxical salivatory responses to chlorosyle and atropine in a denervated human parotid gland.

In the case of the denervated human parotid gland, atropine is a cholinopositive agent that causes an extremely intense and prolonged (up to 3-5 h) salivation. An attempt was made to find out the extent to which the "weight increase" principle had an effect on such a gland, i.e. whether larger analogues of atropine which has a relative molecular mass of 289.4 would stimulate or inhibit the paradoxical salivation. The studies involving chlorosyle of a mass of 355.89 were carried out in seven subjects during the last three years. The cholinopositive activity of chlorosyle, as a ligand with increased weight on both poles, on a denervated gland, was several times lower than that of atropine. With the increase of the ligand's dosage, the cholinoexciting activity of chlorosyle decreased sharply and was just restricted by the initial cholinomimetic excitement transforming into a blockade, which may be compared with the action of depolarizing myorelaxants. The data obtained may provide a foundation for conceptualization of the expansion of a response-active cholinopositive zone in a cholinoreceptor deprived of nervous control, which, probably, results from relocation of hydrophobic segments to the macromolecular periphery or, more precisely, to the synthesis of receptors with another part of the zone. The chlorosyle radicals with increased length and weight, while contacting the hydrophobic segments, conditioned the occurrence of cholinoblocking activity and inhibition of the cholinoexciting effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1973

Salivary reactions after ventromedial hypothalamic lesions in dogs.

Lesions of the ventromedial hypothalamic nucleus produced an increase of food intake and body weight, marked augmentation of intertrial salivation, and transient disinhibition of salivation to the differentiated conditioned stimulus. It is concluded that damage of the ventromedial hypothalamic nucleus produces an increase of alimentary drive.

Animals↗

PubMed1979

The effects of imipramine treatment on the unconditioned alimentary behavior and classical conditioned salivary reactions in dogs.

In Experiment I the effect of imipramine treatment on the unconditioned food intake in dogs was tested. In Experiment II imipramine was injected in dogs in which classical conditioned salivary reflexes had been previously elaborated. Both conditioned and unconditioned salivation were decreased. The differentiation of conditioned salivation to CS+ and CS- was disturbed during the imipramine treatment, due to the prominent decrease of conditioned salivary reflexes to CS+ and also increase of reactions to CS-. Imipramine treatment produced only a slight decrease of food intake. In most dogs of both groups the increase of general arousal and improvement of social contact was observed. The variability of the imipramine effect on particular parameters of alimentary behavior depended on the individual characteristics of each dog. It is concluded that in the evaluation of the effect of imipramine one should take into consideration its differential influences on various motor, autonomic and emotional, central as well as peripheral components of alimentary behavior and characteristics of the individual subjects.

Animals↗

PubMed1983

Predictability of esophageal injury from signs and symptoms: a study of caustic ingestion in 378 children.

The accuracy of signs and symptoms as predictors of the presence and severity of esophageal injury was evaluated in 378 children admitted to three pediatric hospitals between 1970 and 1980. The signs and symptoms analyzed included nausea, vomiting, dysphagia, refusal to drink, abdominal pain, increased salivation, oropharyngeal burns, and abdominal tenderness. The severity of lesions found at esophagoscopy in 378 children was graded from grade 0, no lesion, to grade 3, perforation. Of the 298 patients demonstrating signs or symptoms, 243 (82%) had a grade 0 or 1 lesion, 55 (18%) had a grade 2 lesion, none had a grade 3 lesion, and five (2%) developed a stricture of the esophagus. Among the 80 patients without signs or symptoms, 70 (88%) had a grade 0 or 1 lesion, ten (12%) had a grade 2 lesion, none had a grade 3 lesion, and one (1%) developed a stricture of the esophagus. When individual signs or symptoms were correlated with the severity of esophageal lesion, vomiting (33%) followed by dysphagia (25%), excessive salivation (24%), and abdominal pain (24%) were most frequently associated with a grade 2 or 3 esophageal lesion. A similar percentage of a grade 0 or 1 (82% v 85%), a grade 2 (18% v 15%), and a grade 3 (0%) esophageal lesion followed the ingestion, respectively, of an alkali (324 patients) or an acid (54 patients). In six patients (2%) stricture occurred only following an alkali ingestion. These data demonstrate that signs and/or symptoms do not adequately predict the presence or severity of an esophageal lesion following the ingestion of a caustic substance.

Abdomen↗

PubMed1994

Neurochemical effects of the M1 muscarinic agonist xanomeline (LY246708/NNC11-0232).

Xanomeline [3(3-hexyloxy-1,2,5-thiadiazol-4-yl)-1,2,5,6-tetrahydro-1-me thylpyridine)] was evaluated in vivo in rat brain for effects on neurotransmitter turnover and inhibition of ex vivo binding of muscarinic radioligands. Xanomeline produced dose-related increases in the metabolite of dopamine, dihydroxyphenylacetic acid (DOPAC), in striatum. The increases in striatal DOPAC levels produced by xanomeline were antagonized by the relatively selective M1 antagonist trihexyphenidyl, suggesting that xanomeline interacts with M1 heteroreceptors on dopamine nerve terminals. Xanomeline produced small increases in striatal acetylcholine levels and did not antagonize the large increases in acetylcholine produced by the nonselective muscarinic agonist oxotremorine, indicating that xanomeline did not block M2 autoreceptors. Xanomeline inhibited ex vivo binding of muscarinic radioligands to homogenates of brain and the inhibition of ex vivo binding occurred in the same dose range as increases in DOPAC levels. Xanomeline did not appreciably induce salivation or antagonize oxotremorine-induced salivation indicating that xanomeline does not interact with M3 receptors. The effects of xanomeline on ex vivo binding and DOPAC levels lasted for about 3 hr and were evident after oral administration. An analog of xanomeline with similar in vivo effects did not inhibit acetylcholinesterase or choline acetyltransferase and inhibited choline uptake only at concentrations much higher than those required to inhibit binding. These data indicate xanomeline is selective agonist for M1 over M2 and M3 receptors in vivo in rat. It is not known whether xanomeline interacts with m4 or m5 receptors in vivo.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

An investigation of the vascular organisation of the canine submandibular gland.

It is known that parasympathetic nerve stimulation elevates venous pressure in the dog submandibular gland, and that the venous pressure wave is transformed to that of the arterial pulse. The vascular arrangements and histological characteristics of the dog submandibular gland were therefore examined to establish which anatomical structures are responsible for the change in venous pressure during salivation induced by parasympathetic stimulation. The acinar and ductal circulations were found to be arranged in parallel and arteriovenous anastomoses were identified in both. Microsphere injection studies demonstrated the opening of arteriovenous anastomoses in actively secreting glands. Smooth muscle cells were rarely found in venous blood vessels but venous valves were abundant in both circulations. Dense connective tissue was observed to enclose the ductal system and its accompanying structures (blood vessels, lymphatic vessels and nerves); it was most abundant in the hilum and diminished aborally. The mechanism responsible for elevating venous pressure during parasympathetic salivation is thus probably related to opening of the arteriovenous anastomoses; the increase in the amount of surrounding dense connective tissue in a central direction may facilitate the preservation of the transmitted arterial pressure and pulse in the venous system.

Animals↗

PubMed1996

Serotonin syndrome from venlafaxine-tranylcypromine interaction.

Excessive stimulation of serotonin 5HT1A receptors causes a syndrome of serotonin excess that consists of shivering, muscle rigidity, salivation, confusion, agitation and hyperthermia. The most common cause of this syndrome is an interaction between a monoamine oxidase inhibitor (MAOI) and a specific serotonin reuptake inhibitor. Venlafaxine is a new antidepressant agent that inhibits the reuptake of serotonin and norepinephrine. We report a venlafaxine-MAOI interaction that resulted in the serotonin syndrome in a 23-y-old male who was taking tranylcypromine for depression. He had been well until the morning of presentation when he took 1/2 tab of venlafaxine. Within 2 h he became confused with jerking movements of his extremities, tremors and rigidity. He was brought directly to a hospital where he was found to be agitated and confused with shivering, myoclonic jerks, rigidity, salivation and diaphoresis. His pupils were 7 mm and sluggishly reactive to light. Vital signs were: blood pressure 120/67 mm Hg, heart rate 127/min, respiratory rate 28/min, and temperature 97 F. After 180 mg of diazepam i.v. he remained tremulous with muscle rigidity and clenched jaws. He was intubated for airway protection and because of hypoventilation, and was paralyzed to control muscle rigidity. His subsequent course was remarkable for non-immune thrombocytopenia which resolved. The patient's maximal temperature was 101.2 F and his CPK remained < 500 units/L with no other evidence of rhabdomyolysis. His mental status normalized and he was transferred to a psychiatry ward. This patient survived without sequelae due to the aggressive sedation and neuromuscular paralysis.

Adult↗

PubMed1998

[Clinical findings in 50 cows with bovine spongiform encephalopathy (BSE)].

The goal of this study was to describe the clinical findings in 50 cows with bovine spongiform encephalopathy (BSE). The most important abnormalities were disturbances in behaviour, sensitivity and locomotion. Of 48 cows with behavioural abnormalities, 33 were panic-stricken, 33 were fearful and 32 were restless and nervous. Other behavioural disturbances included bruxism (n = 23), salivation (n = 15), licking of the muzzle (n = 15) and flehmen (n = 8). Hypersensitivity to touching of the head and neck with a pen and reacted by throwing the head sideways, head shaking, curling the muzzle or flehmen and salivating. Hypersensitivity to sound was observed in 41 cows. Hypersensitivity to light was seen in 22 cows. disturbances in locomotion occurred in 44 cows. In 41, there was ataxia, which was generalized in 28 and restricted to the hindend in 13.

Animals↗

PubMed1995

Urodynamic and other effects of tolterodine: a novel antimuscarinic drug for the treatment of detrusor overactivity.

Tolterodine, a novel compound intended for treatment of urgency and urge incontinence, has been characterized as a potent muscarinic receptor antagonist in pharmacological in vitro and in vivo studies. In cats, tolerodine was shown to reduce bladder pressure at doses significantly lower than those affecting salivation. To predict clinical effectiveness, an open pilot study was performed in healthy male volunteers. Efficacy was measured by cystometry and by spontaneously reported effects after administration of a single oral dose of tolterodine, 6.4 mg, given as a water solution. Tolterodine had distinct inhibitory effects on urinary bladder function, both at 1 and 5 hours post-dose. At 1 hour, but not at 5 hours post-dose tolterodine also significantly reduced stimulated salvation. In addition to the objectively demonstrated changes in urodynamic parameters, most volunteers experienced voiding difficulties. No significant changes in blood pressure, heart rate, or near point of accommodation were registered. Tolterodine, in the dosage used, was both objectively and subjectively shown to exert a marked inhibitory effect on micturition in healthy subjects, and the data suggest a more pronounced effect on bladder function than on salivation.

Adult↗

PubMed2000

The role of voltage-gated chloride channels in type II pyrethroid insecticide poisoning.

Pyrethroids act on mammalian sodium channels, but we have previously shown that low concentrations of the type II pyrethroid deltamethrin also decrease the open channel probability (P(o)) of voltage-gated chloride channels. This effect would be expected to amplify the sodium channel-mediated signs of poisoning produced by pyrethroids. In the present study we evaluated potential chloride channel agonists in vitro, and then tested the most effective of these on pyrethroid-poisoned rats to determine the practical significance of chloride channel effects in vivo. Patch clamp experiments showed that, for voltage-gated maxi chloride channels in excised, inside-out patches from mouse N1E 115 neuroblastoma cells, ivermectin (10(-7) M) and pentobarbitone (10(-6) M) significantly increased open channel probability (p </= 0.01 and p </= 0.02, respectively), whereas phenobarbitone, hexobarbitone, mephobarbitone, thiopentone, and barbituric acid did not. This suggested that, if chloride channels were important in vivo, ivermectin and pentobarbitone should antagonize type II pyrethroid poisoning and phenobarbitone should not. Male F344 rats were then pretreated with ivermectin (4 mg/kg iv), equisedative doses of either pentobarbitone (15 mg/kg ip) or phenobarbitone (45 mg/kg ip), or solvent controls. This was followed by deltamethrin (1.5 or 2 mg/kg iv) or the type I pyrethroid cismethrin (4 mg/kg iv). Ivermectin produced a marked fall in deltamethrin-induced salivation (p </= 0.05) and also (in anesthetized rats) in repetitive electromyogram discharge and muscle twitch (p </= 0.01 and p </= 0.05, respectively). Pentobarbitone significantly reduced the motor signs score due to deltamethrin (p </= 0.01). Ivermectin therefore protected against the peripheral signs of deltamethrin poisoning and pentobarbitone protected against the central signs. As expected phenobarbitone had no protective effects. The motor signs produced by the type I pyrethroid cismethrin (which does not act on chloride channels) were not diminished by either barbiturate. The peripheral benzodiazepine receptor blocker PK11195 did not diminish the protective action of ivermectin on the muscle twitch (p </= 0.05), although it partially reversed the block of salivation (p </= 0.05). These results support the hypothesis that the voltage-dependent chloride channel is a toxicologically significant additional site of action for deltamethrin and that the use of chloride channel agonists can provide a rationale for a novel and effective therapy against type II pyrethroid poisoning.

Animals↗

PubMed1979

Methotrexate-induced oral mucositis and salivary methotrexate concentrations.

We examined the plasma and saliva levels of methotrexate (MTX) achieved during the treatment and rescue periods of ten patients receiving 42-h MTX infusions followed by citrovorum rescue. Saliva MTX levels were generally 1%--2% of the simultaneous plasma levels. Four patients developed severe oral mucositis; three patients developed mild to moderate oral toxicity, and three others had no evidence of mucositis. MTX levels in the patients with severe mucositis were not higher and did not persist longer than the levels achieved in patients with mild or absent toxicity. Attempts at reducing the severity of oral mucositis with topical citrovorum mouthwashes or with atropine to suppress salivation were unsuccessful. MTX-induced oral mucositis is not related to salivary MTX concentrations, and the use of topical citrovorum therapy or the suppression of salivation does not appear to ameliorate this toxicity.

Humans↗

PubMed1980

Structure-activity relationships of some pyrethroids in rats.

The intravenous toxicity to the rat of 36 pyrethroids has been examined. With two exceptions they cause either (1) T-syndrome, consisting of aggressive sparring, sensitivity to external stimuli, fine progressing to gross whole body tremor and prostration or (2) CS-syndrome, consisting of pawing and burrowing behaviour, salivation, coarse tremor, progressing to sinuous writhing (choreoathetosis) and clonic seizures. The two exceptions presented a TS-syndrome with salivation associated with the T-syndrome. No clearcut relationship between chemical structure and symptoms of poisoning has emerged through some generalisations are discussed.

Animals↗

PubMed1989

Comparison of the effects of four cholinomimetic agents on cognition in primates following disruption by scopolamine or by lists of objects.

The ability of four central cholinomimetics to reverse a scopolamine-induced spatial memory impairment or to improve visual recognition memory in primates was examined. Physostigmine (0.04-0.08 mg/kg IM) fully reversed the effects of scopolamine (0.03 mg/kg). Coadministration of pilocarpine (3.0-5.0 mg/kg) caused partial reversal of the scopolamine impairment after intermediate or long retention intervals (10 or 20 s). Treatment with arecoline (0.1-1.8 mg/kg) or nicotine (1.0-2.0 mg/kg) generally did not reverse the effects of scopolamine. A task in which memory could be taxed by increasing the number of visual stimuli presented appeared more sensitive to the effects of cholinomimetics on cognition than the scopolamine reversal model. In this paradigm treatment with physostigmine (0.001, 0.01 or 0.03 mg/kg) increased choice accuracy from about 55 to 70% correct. Arecoline improved performance at one dose only (0.1 mg/kg) which also induced marked adverse side-effects (salivation and tremor). Pilocarpine improved performance in the dose range 0.125-0.35 mg/kg, but not at higher doses which also induced marked salivation. Treatment with nicotine (0.001-2.0 mg/kg tended to improve performance but this did not reach statistical significance. The relevance of these findings for studies in man and for animal models of dementia is discussed.

Animals↗