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At least 991 records · Page 55Linked to original sources
PubMed1989

AF-DX 116 discriminates heart from gland M2-cholinoceptors in man.

The M2-cholinoceptor subtype selective antagonist AF-DX 116 was compared with atropine with respect to effects on heart rate and salivary flow in healthy volunteers. These effects were related with in vitro occupancy of M-cholinoceptor subtypes in radioreceptor assays of plasma samples. Radioreceptor assays comprised M1-cholinoceptors in bovine cerebral cortex and M2-cholinoceptors in pig heart and rat salivary gland membranes. 3H-pirenzepine served as a label in the cerebral cortex 3H-N-methyl-scopolamine in the heart and gland preparations. Oral administration of 240 mg AF-DX 116 led to a time dependent increase in heart rate with a maximum effect comparable to atropine 40 micrograms/kg i.v. The effects of both drugs on heart rate were matched by a greater than 80% occupancy of heart M2-cholinoceptors in the radioreceptor assay of plasma samples. In contrast to the complete inhibition of salivary flow after atropine, AF-DX 116 induced an increase of salivation. The effects on salivary flow coincided with a greater than 80% occupancy of glandular M2-cholinoceptors after atropine but no detectable occupancy after AF-DX 116. Occupancy of the M1-subtype amounted to 61.7% after AF-DX 116 and a blockade of inhibitory, presynaptic M1-autoreceptors at missing postsynaptic blockade of glandular M2-cholinoceptors might explain the hypersalivation induced by AF-DX 116.

Adult↗
PubMed1991

Stereoselective effect of morphine on antinociception and endogenous opioid peptide levels in plasma but not cerebrospinal fluid of dogs.

Morphine releases endogenous opioids into the circulation of dogs. To test the stereospecificity of this effect, as well as to determine whether morphine also releases endogenous opioids centrally, which might be involved in its antinociceptive action, the effects of (-)-morphine sulfate (10 mg/kg, sc) or (+)-morphine hydrobromide on antinociception in a dog tail-flick test, on semi-quantified morphine-induced signs of salivation, emesis, defecation and ataxia, and on the plasma and cerebrospinal fluid (CSF) levels of endogenous opioid peptides were studied. Plasma and CSF levels of immunoreactive beta-endorphin (i-BE), met-enkephalin (i-ME), leu-enkephalin (i-LE), and dynorphin (i-DY) were quantified by radioimmunoassay in octadecylsilyl-silica cartridge extracts. Immunoreactive morphine (i-M) levels were measured in unextracted samples. (-)-Morphine treatment significantly increased antinociception, morphine-induced signs, i-M levels in plasma and CSF, and i-BE, i-ME, and i-LE levels in plasma, but not CSF. Levels of i-DY remained constant in plasma and CSF. (+)-Morphine treatment did not alter any of these parameters, indicating that the effects of morphine on nociception, behavioral signs, and plasma endogenous opioids in dogs were stereoselective. It is concluded that morphine does not cause an increase in immunoreactive endogenous opioid peptides in the CSF at the time of its peak antinociceptive effect.

Animals↗
PubMed1992

Physostigmine: dose-response effects on endurance and thermoregulation during exercise.

We previously reported that the administration of 200 micrograms/kg of physostigmine (PH) to rats exercising on a treadmill resulted in decrements in both endurance (decreased running time to exhaustion) and thermoregulation. However, it was necessary to determine the dose-response effects of PH administration before PH-treated exercising rats could be used as a model with which to examine the relative anticholinergic potency of drugs. In the present work saline, 50, 100, or 200 micrograms/kg of physostigmine salicylate (0%, 40%, 50%, and 60% whole blood cholinesterase inhibition) was administered to rats (N = 12/group) prior to treadmill exercise (26 degrees C, 50% rh, 11 m/min, 6 degrees incline). The saline control group ran for 67 +/- 6 min (mean +/- SE) with a rate of rise of core temperature of 0.051 +/- 0.007 degrees C/min. The run times declined (80%, 64% and 48% of control) as rate of rise of core temperature increased (116%, 180%, and 214% of control) in a dose-dependent manner (50, 100, 200 micrograms/kg PH). Cholinergic symptoms such as salivation, tremors, and defecation were also affected in a dose-dependent manner by PH administration. Since cholinergic symptoms, thermoregulatory effects, and endurance decrements all vary in a dose-dependent manner with physostigmine administration, the exercising rat represents a useful model for examining the relative potency of cholinergic therapies.

Animals↗
PubMed1995

Effects of methylecgonidine on acetylcholine-induced bronchoconstriction and indicators of lung injury in guinea pigs.

The fumarate salt of methylecgonidine (MEG; anhydroecgonine methylester), a pyrolysis product of cocaine, has previously been shown to antagonize contractions of guinea pig isolated trachea induced by acetylcholine (ACh) and other spasmogenics. We determined the effects of MEG fumarate on ACh-induced bronchoconstriction in vivo. Specific airway conductance (SGaw) was measured in guinea pigs receiving 30-300 mg/kg s.c. MEG fumarate and exposed one hour later to nebulized ACh (0.2-3.2%; by inhalation). MEG fumarate did not induce any changes in SGaw; neither did it antagonize dose-dependent decreases in SGaw induced by ACh. However, tremors, salivation, startle and increased numbers of fecal boli were observed after MEG administration. Thus, unlike antagonism of ACh-induced contractions of guinea pig isolated trachea observed in vitro, MEG fumarate does not antagonize ACh-induced bronchoconstriction in vivo, even at doses which induced changes in grossly-observable behavior. Inhalation of a condensation aerosol of MEG base induced lung damage as evidenced by the presence of blood and higher levels of protein and lactate dehydrogenase in the lung lavage fluid of MEG-treated animals than of control animals. Aerosols of MEG fumarate, on the other hand, did not induce lung damage when inhaled. These results extend previous observations that MEG base may contribute to detrimental pulmonary effects of crack smoking.

Acetylcholine↗
PubMed1987

Differences in behavioral responses to oxotremorine and physostigmine in New Zealand black (NZB/BlNJ) and C57BL/6 mice.

The NZB/BlNJ (NZB) mice are an autoimmune-prone strain, known to develop brain-reactive antibodies in serum at much earlier chronological ages than normal mice. Measurement of locomotor activity in 8-10 month old C57BL/6 (C57) mice following the administration of either oxotremorine or physostigmine, revealed a biphasic response consisting of inhibition at small doses, but increased motor activity at large doses. In contrast, age-matched NZB mice exhibited little inhibition at the smaller doses, but had much greater increases in activity after the larger doses. Similarly, when compared to C57 mice, NZB mice were less sensitive to oxotremorine-induced salivation, diarrhea and visible tremors. Moreover, oxotremorine-induced hypothermia occurred at smaller doses in C57 mice than in NZB mice and was of a greater magnitude. Thus, at an age when NZB mice possess high levels of brain-reactive antibodies, and exhibit impairment in tests of learning/memory, these mice also show diminished responses in several tests of cholinomimetic-induced behavior and physiological alterations.

Aging↗
PubMed1991

Drugs which stimulate or facilitate central cholinergic transmission interact synergistically with delta-9-tetrahydrocannabinol to produce marked catalepsy in mice.

In experiments in which mice were placed with their forepaws over a 4 cm high horizontal bar, delta-9-tetrahydrocannabinol (THC; 10 mg/kg i.p.) delayed descent from the bar. This effect on descent latency was markedly enhanced by physostigmine (0.05 or 0.25 mg/kg s.c.) and oxotremorine (0.04 or 0.08 mg/kg s.c.), administered immediately before THC. These interactions were attenuated by atropine (2.0 mg/kg s.c.) and (-)-scopolamine (1.9 mg/kg s.c.) but not by atropine methyl nitrate (2.11 mg/kg s.c.), which does not readily cross the blood-brain barrier. However, atropine methyl nitrate did prevent salivation induced by oxotremorine in the presence of THC. No synergism was detected between THC and neostigmine (0.047 mg/kg s.c.). Atropine and (-)-scopolamine also decreased the ability of chlordiazepoxide (10 mg/kg s.c.) to enhance the effect of THC on descent latency. The interaction was not antagonized by atropine methyl nitrate or mecamylamine (1.17 or 2.34 mg/kg s.c.). These results point to an involvement of central acetylcholine-releasing pathways in the cataleptic response of mice to THC.

Acetylcholine↗
PubMed1981

Xerostomia--diagnosis and treatment.

Seventy-one patients complaining of mouth dryness were examined. Decreased salivary rate of flow was found in fifty-six. Twenty-two patients did not respond to stimulation and were treated with artificial saliva. The thirty-four responding patients were treated with a mouthwash containing citric acid (Saliram). Of the patients using Saliram, 91 percent were satisfied with the results, and in 16 percent of these an increase in salivation was observed and persisted after treatment was discontinued.

Aged↗
PubMed1985

Sialographic damage in rat submandibular gland.

The damage caused to rat submandibular glands by intraductal injection was examined. When a small volume of isotonic saline was injected, even if salivation was not influenced, salivary composition was greatly affected because the intercellular junctions of the duct cells were damaged. Intraductal injections of hyperosmotic solutions or highly viscous liquids were more effective in damaging intercellular junctions. When interpreting the significance of a salivary composition in clinical diagnosis, it is necessary to consider the sialographic damage which might influence the salivary composition.

Animals↗
PubMed1988

Salivary gland function in patients on chronic lithium treatment.

Salivary gland function was studied in 14 manic-depressive patients treated with lithium carbonate (Li) for 4 to 120 months. Function level was evaluated by means of sialometry, dynamic salivary scintigraphy, and sialography. Daily Li dose, serum Li concentration, duration of Li therapy, and caries activity index were correlated with the salivary function parameters studied. Hyposalivation was noted in 71% of the patients, showing good correlation with the scintigraphic (r = 0.94) and sialographic (r = 0.87) results. Duration of Li therapy was poorly correlated with the degree of salivary gland dysfunction and with the caries activity index, whereas the correlation between duration of therapy and each of the three salivary function parameters was erratic. Because four of the patients exhibited normal salivation, we suggest that there are some additional factors (e.g., genetic or thyroid function level) that might be involved in salivary dysfunction connected with Li therapy.

Adult↗
PubMed1989

Episodic supersalivation (idiopathic paroxysmal sialorrhea): description of a new clinical syndrome.

Four patients have been identified as experiencing a form of sialorrhea not previously described in the dental literature. The pattern of salivation is atypical in that it is excessive and is episodic in nature, with paroxysms of secretion occurring 1 to 2 times per week and lasting for 2 to 5 minutes. The episodes are preceded by a prodrome consisting of nausea or epigastric pain, but without progression to vomiting. Because of the unknown cause and spontaneous occurrence, the syndrome is being called idiopathic paroxysmal sialorrhea (IPS).

Aged↗
PubMed1993

Pilocarpine and other cholinergic drugs in the management of salivary gland dysfunction.

Sialagogues constitute an important component in the management of salivary gland dysfunction. Of the pharmacologic agents available, pilocarpine has been used extensively over the last century. Many clinical trials have documented the efficacy of this alkaloid, with doses that range from 1 to 15 mg normally taken four times a day. There is considerable individual variation in response although it is usually possible, in the presence of sufficient responsive exocrine tissue, to establish a therapeutic regimen that promotes increased salivation without significant side effects.

Anethole Trithione↗
PubMedDate not supplied

An estimation of the number of malaria sporozoites ejected by a feeding mosquito.

Restrained Anopheles stephensi mosquitoes infected with Plasmodium falciparum were made to produce time-dependent series of saliva droplets in mineral oil. The relative volume of each droplet and the number of sporozoites each contained were determined microscopically; gland sporozoites were estimated with an enzyme-linked immunosorbent assay. Median gland infection was 8170 and median number of sporozoites ejected was 15 (range, 0-978). Inoculum size was positively correlated to the number of sporozoites in the salivary glands. Most mosquitoes ejected sporozoites only at the beginning of salivation; this suggests that only those parasites in the common and secondary salivary ducts at the time of feeding can be ejected. The small size of inocula may explain some aspects of malaria transmission, including the often observed discrepancy between inoculation and incidence rates.

Animals↗
PubMedDate not supplied

Detecting malaria sporozoites in live, field-collected mosquitoes.

A method is described for identifying malaria-infected mosquitoes, without killing them or hampering their fitness. Individual mosquitoes were induced to salivate on coverslips, and sporozoites, deposited on the glass surface, were visualized by Giemsa staining. Of 21 mosquitoes found to contain sporozoites by salivary gland dissection, 13 had delivered sporozoites on coverslips. A positive correlation was found between the amount of saliva expelled and ejection of sporozoites, indicating that the sensitivity of the method may be increased by improving the probing behaviour of the mosquitoes. The procedure described may be suitable for selecting infected mosquitoes which are able to eject sporozoites during probing. Being applicable to wild Anopheles and to large numbers of mosquitoes, the method lends itself for use in field studies on malaria.

Animals↗
PubMed1986

Acute and subchronic toxicity of a nonsulfhydryl angiotensin-converting enzyme inhibitor.

Acute and 1-month toxicity studies with SCH 31846, a nonsulfhydryl anti-hypertensive agent which acts by inhibiting angiotensin-converting enzyme, were initiated to evaluate its toxicity. The oral LD50s in mice and rats were approximately 1.8 and 2.5 g/kg, respectively, while the iv LD50 was approximately 450 mg/kg in mice and 150 mg/kg in rats. Signs of acute toxicity in rats and mice included salivation, hypoactivity, ataxia, prostration, and convulsions. In a 1-month dog study at oral doses of 25, 75, or 150 mg/kg, there was a dose-related increase in emesis between 1 and 2 hr after dosing. Absorption studies showed peak blood concentrations occurring in dogs between 0.3 and 1 hr after dosing. No other noteworthy antemortem changes were observed. In a 1-month rat study at oral doses of 30, 180, or 600 mg/kg, the hematocrit and hemoglobin values of the 600 mg/kg-dosed female rats were slightly but significantly (p less than 0.05) decreased and the blood urea nitrogen was slightly but significantly (p less than 0.05) increased in all SCH 31846-dosed male rats and the 600 mg/kg-dosed female rats. Absorption studies in male rats at doses of 30, 180, and 600 mg/kg indicate that SCH 31846 is well absorbed in rats. The 150 mg/kg-dosed dogs and the 180- and 600 mg/kg-dosed rats had a slight increase in the number of renin-containing granules in the renal juxtaglomerular cells. No other compound-related microscopic changes were observed. These data are similar to data reported for Captopril and suggest that in the dog and rat the toxicity of ACE inhibitors is not dependent upon the presence or absence of a sulfhydryl group.

Administration, Oral↗
PubMed1990

Characteristics of the prolonged inhibition produced by a range of pyrethroids in the rat hippocampus.

Eight different synthetic pyrethroids were examined to determine their effects on the excitability of hippocampal granule cells in urethane-anesthetized rats. A paired stimulus approach was used. All eight prolonged the depression of granule cell excitability that follows stimulation of their major synaptic input, the perforant path. The magnitude of this effect depended upon the class to which the pyrethroid belonged. Type I pyrethroids (those primarily producing tremor) prolonged the depression of granule cell excitability for shorter periods than did type II pyrethroids (those primarily producing salivation and choreoathetosis) or pyrethroids producing a mixed type of intoxication. No overlap was found between groups. To determine whether the difference observed between type I and type II pyrethroids was the result of an infelicitous selection of doses, cismethrin (type I) was tested over a dose range of 1.5-24 times the conscious rat iv LD50. Even at the highest dose, the prolongation remained well below that produced by type II pyrethroids. The effect of deltamethrin was shown to be consistent with the production or potentiation of a surmountable inhibitory response. This action of deltamethrin was antagonizable by mephenesin and lidocaine, but not by picrotoxin or halothane. The type of effect, its time course, and the antagonism data suggest that type II pyrethroids enhance inhibition in the dentate gyrus. This action does not appear to be mediated by GABAA receptors.

Animals↗
PubMed1992

Prophylactic and therapeutic efficacy of memantine against seizures produced by soman in the rat.

Male Sprague-Dawley rats injected sc with a single sublethal dose of the organophosphate nerve agent, soman (100 micrograms/kg), had motor limbic seizures within 5-15 min. Pretreatment with a single dose of memantine HCl (MEM, 18 mg/kg, sc), alone or in combination with atropine sulfate (ATS, 16 mg/kg, sc), before soman prevented seizures without sedation or ataxia. Rats appeared normal or demonstrated increased exploratory activity. Excessive salivation, a peripheral manifestation of soman intoxication, was decreased by ATS, but pretreatment with ATS alone did not prevent seizures. After seizure onset, MEM +/- ATS, but not ATS, abolished seizures. Acetylcholinesterase (AChE) activity in several brain regions (cortex, stem, striatum, and hippocampus) was markedly reduced by soman, but not by MEM, ATS, or MEM + ATS. Preadministration of MEM + ATS in vivo significantly protected AChE from inhibition by soman. Memantine reduced inhibition of AChE activity in crude brain homogenates by soman, but not by edrophonium (anionic site inhibitor) or decamethonium (peripheral site inhibitor). Thus, MEM may bind to a different modulatory site, not yet characterized, to protect AChE. When given after onset of soman-induced seizures, treatment with MEM +/- ATS did not reactivate AChE although seizures were controlled, suggesting additional anticonvulsant mechanisms of action. At concentrations (10(-4) to 5 x 10(-4) M) which did not significantly alter the spontaneous firing of action potentials (APs), MEM limited sustained high frequency repetitive firing (SRF) induced by depolarization of spinal cord (mouse and rat) and neocortical (mouse) neurons in monolayer-dissociated cell culture. In the same range of concentrations, ATS both limited SRF and suppressed spontaneous activity, suggesting toxicity. In addition, MEM and ATS reversibly produced use-dependent block of depolarizing responses to acetylcholine (ACh) applied by pressure ejection to spinal cord neurons. Thus, the anticonvulsant efficacy of MEM, with or without ATS, may have resulted from a combination of actions, including protection of AChE from inhibition by soman, limitation of high frequency firing of APs, and blockade of excitatory postsynaptic responses to ACh.

Animals↗
PubMed1983

Effects of scorpion and rattlesnake venoms on the canine pancreas following pancreaticoduodenal arterial injections.

Three scorpion venoms caused a transitory decrease in the rate of fluid secretion and increases in the concentration, in pancreatic juice, of total protein and individual enzymes. Protein and enzyme elevations 4-7 fold over the basal levels were produced by the venom of Tityus bahiensis and 6-7 fold by venoms from Tityus serrulatus and Buthus quinquestriatus. Although these increases were smaller than those stimulated by the C-terminal octapeptide of cholecystokin (OP-CCK; 8-9 fold), the secretory responses were of longer duration, so that the total output of protein caused by each of the three venoms was significantly greater than that observed with OP-CCK. Although electron microscopy revealed evidence of widespread degeneration of acinar cells at 1 hr and more extensive damage at 2 hr following injection of scorpion venom, no free protease was detected in pancreatic secretion collected during this period. The scorpion venoms also caused hypersecretion of viscid saliva. In contrast, rattlesnake venom, had no detectable effect on salivation, pancreatic secretion or morphology of the pancreas.

Animals↗
PubMed1978

Tracheobronchial irritancy of inhaled prostaglandins in the conscious cat.

A novel test was developed to measure the tracheobronchial irritant activity of inhaled prostaglandins. Conscious restrained cats were challenged with separate aerosols of PGE1, PGF2alpha, acetylcholine or isoprenaline. All of the aerosols except isoprenaline caused coughing in a concentration related manner. Tolerance developed very quickly to the tracheobronchial irritation and lasted 1-2 days for PGE1 and less than 1 day for PGF2alpha and acetylcholine. When a 3 day interval between each aerosol challenge was used, PGF2alpha was approximately 700 times more potent than acetylcholine as a tracheobronchial irritant. The highest PGE1 aerosol concentration (500microgram/ml) also caused sedation, diarrhoea and salivation. This test probably provides a useful method for evaluating the tracheobronchial irritant activity of potential prostaglandin bronchodilator analogues and for investigating the mechanism of action of prostaglandin induced tracheobronchial irritancy.

Acetylcholine↗