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At least 307 records · Page 17Linked to original sources
PubMed1980

New methods used to investigate the control of mucus secretion and ion transport in airways.

Our group developed two in vivo methods to study secretions from submucosal glands in exposed tracheal epithelium. (1) The exposed mucosal surface was coated with powdered tantalum; accumulated secretions produced elevations (hillocks) in the tantalum layer under which the duct openings were located. The rate of formation of the hillocks was observed through a dissecting microscope, and recorded by television on a video tape recorder. (2) Micropipets were used to collect timed samples from individual gland duct openings. With these techniques, the innervation of the submucosal glands and the autonomic regulation of their secretions were studied. We studied the control of ion movement across tracheal epithelium because active ion transport forms local osmotic gradients across epithelia which could regulate transepithelial water movement. We mounted pieces of the posterior wall of dog trachea in Ussing-type chambers and measured unidirectional fluxes of Cl- and Na+ under short-circuit conditions with 36Cl and 24Na. We found active transport of Cl- toward the lumen and Na+ toward the submucosa. With this technique we investigated the effect of parasympathomimetic drugs on ion movement. With a new in vitro method we studied output of 35S bound to sulfated mucins and movement of ions in cat trachea. We mounted pieces of anterior tracheal wall in Ussing-type chambers, added sodium 35S-sulfate to the submucosal side and monitored secretion of bound 35S in samples from the luminal side after dialysis. The unidirectional fluxes of Cl- and Na+ were measured with 36Cl and 22Na. With this method we examined the effect of alpha-adrenergic and beta-adrenergic agonists on mucin secretion and ion movement. Also with this preparation we studied the relationship between the permeability of the paracellular pathway to 14C-sucrose and the pattern of tight junction strands.

Animals↗
PubMed2002

Medical backgrounders: glaucoma.

Glaucoma is a leading cause of irreversible blindness in the world. Currently, glaucoma is diagnosed as a progressive optic neuropathy with characteristic optic disc and nerve fiber layer damage, usually associated with loss of visual function. The intraocular pressure (IOP) is the most important risk factor for the disease, although a significant proportion of patients do not have elevated IOP. Other risk factors include older age, African descent, myopia and family history of the disease. The ophthalmoscopic examination of the optic disc is essential to identify the signs of glaucomatous optic neuropathy, such as increased cupping, neuroretinal rim thinning or optic disc hemorrhages. Glaucomatous visual field loss usually starts in the periphery, and loss of central vision does not occur until late in the course of the disease. Visual function is most commonly assessed by standard automated perimetry; however, as many as 50% of nerve fibers can be lost before the appearance of visual field defects in this test. Newer technologies have been developed to find more sensitive ways to detect early glaucoma using both functional (short-wavelength automated perimetry and frequency-doubling perimetry) and structural (scanning laser topography, optical coherence tomography and scanning laser polarimetry) measurements. The management of glaucoma is based on lowering the intraocular pressure to prevent further optic nerve damage. Currently, there are five major classes of medications that are used to lower the intraocular pressure: Beta-adrenergic antagonists, adrenergic agonists, parasympathomimetics, prostaglandin-like analogues and carbonic anhydrase inhibitors. The goal of therapy is to maintain adequate vision for patients during their lifetime, keeping in mind the possible adverse effects of the drugs. If additional lowering of IOP is indicated or if medication fails to sufficiently lower the IOP, laser trabeculoplasty is usually the next step. If IOP is still not adequately controlled, incisional glaucoma surgery is indicated. Neuroprotective agents, which directly protect the optic nerve in glaucoma, are being evaluated in clinical trials.

Glaucoma↗
PubMed1983

Inhalation challenge with carbachol and isoproterenol to predict bronchospastic response to propranolol in COPD.

Disabling propranolol-induced bronchospasm occasionally prevents use of this drug in patients with chronic obstructive pulmonary disease (COPD). A means was developed to identify patients who have high risk for this adverse effect using bronchial challenge by inhaling the parasympathomimetic drug, carbachol, and isoproterenol. After baseline pulmonary function tests, 12 patients with varying degrees of COPD and 13 control patients underwent maximal beta-blockade using intravenously administered propranolol during cardiac catheterization followed by repeat pulmonary function testing. Seven of the patients with COPD and ten of the control subjects were restudied while taking propranolol orally for at least three weeks. The results indicated that the bronchodilator response to inhaled isoproterenol does not reliably identify patients who develop bronchoconstriction with propranolol, but bronchoconstriction after inhaling carbachol is indicative of the high risk of developing bronchoconstriction from propranolol.

Bronchial Spasm↗
PubMed1982

Islet-activating protein (IAP) reduces bethanechol-stimulated release of pancreatic polypeptide in the dog.

The effect of islet-activating protein (IAP) purified from culture medium of Bordetella pertussis was examined in dogs. This was assessed by the levels of pancreatic polypeptide (PP) as well as the responses of plasma insulin and glucagon to a parasympathomimetic agent, bethanechol. Plasma responses of these pancreatic hormones were measured before and 5 days after IAP injection. Although IAP had no significant effect on the bethanechol-stimulated increase in plasma glucose, insulin and glucagon, the PP response to bethanechol was significantly reduced after IAP treatment compared with that before IAP (p less than 0.05). In conclusion, IAP significantly and selectively reduced bethanechol-stimulated PP release in the dog although the mechanism remained to be elucidated.

Animals↗
PubMed1999

Cholinergic stimulation with pyridostigmine, hemodynamic and echocardiographic analysis in healthy subjects.

OBJECTIVE: Growing evidence suggests that sudden death after an acute myocardial infarction (AMI) correlates with autonomic nervous system imbalance. Parasympathomimetic drugs have been tested to reverse these changes. However, their effects on ventricular function need specific evaluation. Our objective was to analyze pyridostigmine's (PYR) effect on hemodynamic and echocardiographic variables of ventricular function. METHODS: Twenty healthy volunteers underwent Doppler echocardiographic evaluations, blood pressure (BP), and heart rate (HR) assessment at rest, before and 120 min after ingestion of 30 mg PYR or placebo, according to a double-blind, placebo-controlled, crossed and randomized protocol, on different days. RESULTS: PYR was well tolerated and did not cause alterations in BP or in ventricular systolic function. A reduction in HR of 10.9 +/- 1.3% occurred (p < 0.00001). There was an A wave reduction in the mitral flow (p < 0.01) and an E/A ratio increase (p < 0.001) without changes in the other diastolic function parameters (p > 0.05). CONCLUSION: PYR reduces HR and increases E/A ratio, without hemodynamic impairment or ventricular function change.

Adult↗
PubMed1980

Changes in the adenohypophysis and genital tract of cryptorchid rats: some morphological and pharmacological aspects.

It has been confirmed that cryptorchidism may affect the control mechanism of gonadotrophin secretion. This has been based on morphological aspects of the adenohypophysis of cryptorchid rats which have shown an increase in basophilic and vacuolated basophilic cells, an increase known to be related to the production of gonadotrophin. The morphological alterations observed in the testes, prostates, seminal vesicles and ductus deferentes of these cryptorchid animals, the quiescence and the responses of their seminal vesicles and ductus deferentes to sympathomimetic and parasympathomimetic drugs indicated that these cryptorchid animals may be somewhere between normal and castrated rats, although not equidistant from either. Comparison of wet weights and of occurrence of spontaneous contractions, and determination of drug parameters in seminal vesicles and ductus deferentes taken from normal, castrated or crptorchid rats, suggested that the development and the spontaneous or the pharmacological responses of male accessory organs of reproduction are independent phenomena.

Acetylcholine↗
PubMed1982

Regulation of plasma immunoreactive glucagon in obese hyperglycaemic (ob/ob) mice.

This study examines the role of glucagon in the pathogenesis of the obese hyperglycaemic (ob/ob) syndrome in mice. Plasma C-terminal immunoreactive glucagon concentrations were measured in fed and fasted ob/ob mice at different ages between 5-40 weeks, and in 20-week-old mice after the administration of established stimulators and inhibitors of glucagon secretion. Plasma glucagon concentrations were inappropriately raised irrespective of age, nutritional status and the accompanying prominent changes in plasma glucose and insulin concentrations. Glucose suppressed plasma glucagon in the fed but not the fasted state, suggesting a dependence on the marked hyperinsulinaemia associated with feeding. Administration of 0.25 units insulin/kg to fasted mice failed to affect plasma glucagon and glucose concentrations. Increasing the dose to 100 units/kg restored the normal suppressive actions of insulin. Fasted mice showed an exaggerated glucagon response to arginine but not to the parasympathomimetic agent pilocarpine. Fed mice displayed normal plasma glucagon responses to the sympathomimetic agents noradrenaline and adrenaline. Administration of insulin antiserum or 2-deoxy-D-glucose raised plasma glucagon concentrations of fed mice. Contrary to the lack of suppression by glucose in the fasted state, heparin-induced increase in free fatty acids reduced plasma glucagon concentrations. This study demonstrates inappropriate hyperglucagonaemia and defective A-cell function in ob/ob mice. The extent of the abnormality is exacerbated by fasting and appears to result from insensitivity of the A-cell to the normal suppressive action of insulin.

Animals↗
PubMed1999

Xerostomia and hyposalivation: causes, consequences and treatment in the elderly.

Xerostomia and salivary gland hypofunction (SGH) are prevalent in elderly populations, causing much discomfort and even difficulties in eating. SGH also increases the occurrence and severity of oral diseases and makes the patient susceptible to candidiasis. The principal causes of SGH and xerostomia are systemic diseases and drugs used daily. The diagnosis of SGH and xerostomia is based on simple methods, of which measuring both unstimulated and stimulated salivary flow rate is the most important. Treatment calls for proper management of underlying disease, avoidance of all unnecessary medications, and topical remedies such as artificial saliva substitutes. However, good hydration is essential in the elderly with SGH and xerostomia, and water is the drink of choice. In extremely difficult cases, for instance in patients receiving radiotherapy for cancer of the head and neck regions, parasympathomimetic drugs may be administered if no contraindications exist.

Aged↗
PubMedDate not supplied

Interpretation of the serum digoxin concentration.

Significant problems exist in the interpretation of serum digoxin concentration data. Failure to distinguish between results that do not require precise clinical correlation (proof of absorption, presence of drug, etc) and those which depend upon clinical correlation for their meaning ('toxicity' or 'effectiveness') can result in interpretive errors. Problems relating to the source of the serum digoxin concentration can also confound interpretation. Such difficulty may be controllable (obtaining the sample at the proper time, haemolysis, etc) or related to the laboratory technique (cross-reactivity with digoxin metabolites or other medications, technical errors, or lack of precision). Variation within the same patient over time or between patients related to disease (alterations in electrolytes, adrenergic or parasympathomimetic tone, or other medications) may prevent the direct attribution of an observed phenomenon to a particular digoxin concentration. Techniques for determining the effect of digoxin do exist and can be used to gather data for clinical correlations. Ways of improving the interpretaion of serum digoxin concentrations also exist and should be used to improve their value in patient management. The serum digoxin concentration seems to have an important future role. However, we need to know how better to interpret and exploit serum digoxin concentration data.

Adenosine Triphosphatases↗
PubMed1988

Current concepts in the treatment of disorders of micturition.

Disorders of micturition may be divided into disturbances of the storage function of the bladder, and disturbances of the emptying function. The main symptoms of disturbances of storage function are frequency, urgency and incontinence. Hyperactivity of the bladder may lead to urge incontinence, and incompetence of the urethral closure mechanism to stress incontinence. There are many drugs available for treating bladder hyperactivity, but their efficacy as judged from controlled clinical trials (when available) is often limited. Bladder contraction in man is mediated by stimulation of muscarinic receptors, and when given parenterally anticholinergic drugs have been shown to depress bladder hyperactivity irrespective of the underlying cause. Clinically, however, treatment of urge incontinence with anticholinergic drugs is often unsatisfactory. Lack of effect of oral treatment and systemic side effects limit the use of available agents. Drugs with "mixed" actions (anticholinergic and 'direct' muscle effects), for example oxybutynin and terodiline, have well-documented efficacy in bladder hyperactivity. Side effects are common with oxybutynin; terodiline seems to be well tolerated. The aim of drug treatment of stress incontinence is to increase outflow resistance. Although there is only limited possibility of improving the condition with drugs, beneficial effects can be obtained in some patients by use of orally active alpha-adrenoceptor agonists (e.g. phenylpropanolamine) and/or oestrogens. The main symptom of disturbed bladder emptying is urinary retention. Drug therapy is aimed at improving the contractile activity of the detrusor or reducing urethral outflow resistance. Drugs used for improving bladder contractility include parasympathomimetic agents, e.g. bethanechol or carbachol, and intravesical instillation of prostaglandins. Although the efficacy of both types of treatment is open to question, bethanechol seems to be widely used. Increased outflow resistance may be seen in patients with parasympathetic decentralization of the lower urinary tract or in patients with benign prostatic hypertrophy. These patients may respond favourably to alpha-adrenoceptor blockers such as phenoxybenzamine or prazosin.

Humans↗
PubMed1991

New developments in the drug treatment of glaucoma.

This article reviews standard treatment modalities for patients with glaucoma and describes 3 classes of drugs which are undergoing development: apraclonidine (aplonidine, ALO 2145), an alpha 2-adrenergic agonist which has been released for clinical use; topical carbonic anhydrase inhibitors, a modification of the systemic carbonic anhydrase inhibitors currently in use; and prostaglandins (PGs), a new class of drugs with topical ocular hypotensive activity. Standard treatment modalities include parasympathomimetic agents such as pilocarpine, carbachol, and phospholine iodide, which lower intraocular pressure (IOP) by increasing aqueous outflow through the trabecular meshwork. A newer form of pilocarpine as a gel produces a longer action. Adrenergic agonist medications, such as epinephrine (adrenaline) and its prodrug dipivefrine (dipivalyl epinephrine), function by increasing uveoscleral outflow and trabecular outflow facility. A decrease in aqueous formation by the ciliary processes is thought to be the mechanism of action of beta-adrenoceptor antagonists, but the physiological basis for this action has not been clearly demonstrated. A newer beta-blocker, betaxolol, has relatively selective beta 1-blocking activity. Carbonic anhydrase inhibitors are nonbacteriostatic sulphonamide derivatives which decrease aqueous formation by the ciliary body. Almost 50% of patients taking these medications are unable to tolerate them because of their adverse effects, and there is thus much interest in the development of a topical carbonic anhydrase inhibitor with the potential for fewer adverse effects. MK 507 is the most recent and most potent compound in the series of topically active carbonic anhydrase inhibitors. Apraclonidine hydrochloride is a derivative of clonidine hydrochloride, an alpha 2-adrenergic agonist. Clonidine has previously been shown to lower IOP significantly, but has the potential to produce marked lowering of both systolic and diastolic blood pressures. Its major ocular effect appears to be a decrease in aqueous production. The structural modification to apraclonidine decreases corneal absorption and the drug's ability to cross the blood-brain barrier, minimising the risk of centrally mediated cardiovascular side effects. Apraclonidine may also influence secondary avenues of aqueous outflow, such as uveoscleral outflow, and may also affect conjunctival and episcleral vascular flow. It produces a mean decrease in IOP of 25% for as long as 12 hours. Adverse effects include blanching of the conjunctiva, minimal mydriasis and eyelid retraction. This drug has been approved in the US for use in prevention of elevated IOP after argon laser trabeculoplasty and iridotomy, and has potential uses in preventing an IOP rise after YAG laser posterior capsulotomy and cataract surgery in patients already on other antiglaucomatous medications.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Agonists↗
PubMed2006

Use of neostigmine in the management of acute postoperative pain and labour pain: a review.

Neostigmine is a parasympathomimetic agent that has been recently investigated for use as an adjunct analgesic agent in the perioperative and peripartum period. A number of studies have investigated the intrathecal, epidural, caudal and intra-articular routes of administration of this agent, as well as the addition of neostigmine to local anaesthetics used for brachial plexus block and intravenous regional anaesthesia. While the intrathecal administration of neostigmine produced useful analgesic effects in the postoperative period in some studies, the high incidence of adverse events, mainly nausea and vomiting, limit the clinical usefulness of this route of administration. Several studies investigated the postoperative analgesic effects of epidural neostigmine using a number of different regimens. Overall, this route of administration appeared to improve postoperative analgesia in most studies without increasing the incidence of adverse events, and merits further research. Neuraxial administration of neostigmine appears to be safe in the obstetric population, with no reported adverse effects in the mother or fetus. While intrathecal administration is limited by a high incidence of nausea and vomiting in this patient population, the epidural route appears more promising and requires further investigation. The addition of neostigmine to caudal local anaesthetics was associated with improved postoperative analgesia in a number of studies. A dose of 2 microg/kg proved to be effective in several studies but was associated with an increased incidence of vomiting in some studies. Intra-articular administration of neostigmine 500microg produced a useful analgesic effect in the postoperative period in several studies and was not associated with an increase in the incidence of adverse effects. Studies investigating the efficacy of adding neostigmine to the local anaesthetics used for brachial plexus block and intravenous regional anaesthesia reported conflicting results. Further studies are required to determine the place of the administration of neostigmine by these routes.

Anesthesia, Conduction↗
PubMed2002

Muscarinic receptors as a target for drugs treating schizophrenia.

The family of 5 muscarinic acetylcholine receptors belongs to the superfamily of G protein coupled neurotransmitter receptors that serve in part as regulators of synaptic function. Muscarinic receptors are anatomically positioned in cortical and subcortical areas and modulate dopaminergic and glutamatergic neurotransmission thought to be dysfunctional in schizophrenia. Neurochemical studies have shown that dopamine and muscarinic receptors reciprocally modulate one another. For example, the muscarinic agonist xanomeline increases extracellular levels of dopamine and Fos expression in cortical areas greater than subcortical areas, similar to effects of atypical antipsychotics. In electrophysiological studies, xanomeline with acute and chronic administration decreased firing of the mesocorticolimbic dopamine A10 tract, but not the motoric dopamine A9 tract. Behavioral investigations have shown that muscarinic agonists, like dopamine antagonists, inhibit conditioned-avoidance responding and dopamine-agonist-induced behaviors including hyperactivity, climbing behavior and disruption of prepulse inhibition, models for positive symptoms of schizophrenia. Transgenic knockout mice lacking M(4) receptors are hyperactive and hyper-responsive to dopamine D(1) agonists, suggesting a dynamic balance between the dopamine and M(4) receptors. Muscarinic agonists had activity in animal models of negative symptoms, cognitive dysfunction and affective disorders, symptoms that are prominent in schizophrenic patients. Consistent with effects in animal models, preliminary clinical investigation indicates that muscarinic agonists like xanomeline may be effective in the pharmacotherapy of schizophrenia. Thus, we hypothesize that a combined M(1) agonist to promote cognition and a M(4) agonist for antipsychotic-like effects would treat the symptom domains of schizophrenia without parasympathomimetic side effects.

Animals↗
PubMed2000

Use of cis-bis-neodecanoato-trans-R,R-1,2-diaminocyclohexane platinum (II), a liposomal cisplatin analogue, in cats with oral squamous cell carcinoma.

OBJECTIVE: To determine clinical response and toxic effects of cis-bis-neodecanoato-trans-R,R-1,2-diaminocyclohexane platinum (II) (L-NDDP) administered i.v. at escalating doses to cats with oral squamous cell carcinoma (SCC). ANIMALS: 18 cats with oral SCC. PROCEDURE: Cats that failed to respond to conventional treatment or had nonresectable tumors were included. Data included a CBC, serum biochemical analyses, urinalysis, cytologic examination of a fine-needle aspirate of enlarged lymph nodes, and thoracic and oral radiographs for clinical staging. A starting dose (75 to 100 mg/m2 of L-NDDP) was administered i.v.. At 21-day intervals, subsequent doses increased by the rate of 5 or 10 mg/m2. Response was evaluated every 21 days by tumor measurement and thoracic radiography. Quality of life was assessed by owners, using a performance status questionnaire. RESULTS: On average, cats received 2 treatments. Toxicoses included an intermittent, acute anaphylactoid-parasympathomimetic reaction, lethargy or sedation (< or = 24 hours), inappetence or signs of depression (< or = 72 hours), mild to moderate increase in hepatic enzyme activity, and melena. Pulmonary, renal, or hematopoietic abnormalities were not evident. Performance status surveys indicated normal behavior and grooming or decreased activity and self-care (19/20 assessments), ate well with or without assistance (15/20), and did not lose weight (15/20). Median survival time was 59.8 days (mean, 54.1 days). CONCLUSIONS AND CLINICAL RELEVANCE: L-NDDP was ineffective for treatment of cats with oral SCC. None of the cats had a complete or partial remission. Acute toxicoses and poor therapeutic response limit therapeutic usefulness of L-NDDP in cats, unless dosage, frequency, and administration procedures can be improved.

Animals↗
PubMed1988

Bethanechol chloride as a suggested adjunct to prolonged in vivo exposure therapy in the treatment of paruresis.

A major difficulty in treating paruresis (psychogenic urinary retention) by prolonged in vivo exposure therapy involves the individual's inability to initiate urination in response to anxiety-provoking stimuli easily and frequently enough to generalize the desired behavior to everyday situations. Administration of bethanechol chloride, a parasympathomimetic compound that facilitates urination by prompting contraction of the detrusor muscle of the bladder, prior to therapeutic sessions is suggested to enhance the efficiency and effectiveness of in vivo desensitization procedures in the treatment of paruresis.

Behavior Therapy↗
PubMed1983

Postvagotomy acid secretion and mucosal blood flow during beta-adrenoceptor stimulation and universal chemical sympathectomy in dogs.

The aim of the present study was to examine the effect of beta-adrenoceptor stimulation, alpha blockade, and elimination of the adrenergic nerve function on mucosal blood flow and acid secretion in parietal-cell-vagotomized (PCV) gastric fistula dogs. Isoprenaline inhibited pentagastrin-stimulated gastric acid secretion via the beta 1 receptors non-competitively. The effect of isoprenaline was more pronounced after vagotomy than before vagotomy and significantly more pronounced than the effect on parasympathomimetically stimulated (bethanechol) gastric acid secretion. The animals were subjected to chemical sympathectomy with 6-hydroxy-dopamine, a false neurotransmitter that selectively destroys the adrenergic nerve terminals. Chemical sympathectomy increased the pentagastrin-stimulated gastric acid secretion and stabilized the mucosal blood flow at the level before vagotomy, but with an increased ratio between blood flow and acid secretion. One may conclude that the sympathetic nerve system influences gastric function after vagotomy.

Adrenergic beta-Agonists↗
PubMed1987

Pharmacology of converting enzyme inhibitors.

Angiotensin converting enzyme inhibitors were developed to prevent the in vivo generation of angiotensin II and thereby to reduce peripheral vasoconstriction. However, these compounds exert some additional effects that may or may not be angiotensin dependent. These include potential sodium diuresis, bradykinin accumulation, prostaglandin release, blunting of sympathetic activity, parasympathomimetic actions, central effects, redistribution of blood flow toward some particularly important organs. Only the comprehensive assessment of the many complex interactions that exist between the renin-angiotensin and several other regulatory systems reveals the complete therapeutic profile of this class of pharmacologic agents.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Effects of carbamylcholine and isoproterenol on electrolyte fluxes in perfused main duct of submandibular gland of reserpinized rat.

Administration of reserpine (RES) at a dosage of 0.5 mg/kg body wt, ip daily for 7 days was found to lower the dose of carbamylcholine and isoproterenol that alters sodium and potassium transport by cells of the main duct of rat submandibular gland. In the perfused main excretory duct of the submandibular gland of the RES rat, administration of carbamylcholine at a dosage of 1 microgram/kg body wt, inhibited net efflux of sodium (17%) and administration of isoproterenol at a dosage of 2 micrograms/kg body wt increased net efflux of sodium (20%); these drugs, at the same dosages, did not induce significant change in electrolyte flux of normal rat. At a dosage of 5 micrograms/kg body wt, carbamylcholine decreased net influx of potassium (15%) in the RES rat but was without effect on normal rat. Isoproterenol at the dosage of 5 micrograms/kg body wt significantly inhibited net influx of potassium in both the RES rat and normal rat. The data suggested that the duct cells developed supersensitivity to sympathomimetic and parasympathomimetic stimulation after chronic RES treatment.

Animals↗