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At least 343 records · Page 19Linked to original sources
PubMed1989

Studies on the salivary secretion induced by substance P in perfused submandibular gland of rat.

The purpose of these experiments was to clarify the effects of substance P (SP) on the salivary secretion in comparison with those of autonomic agents. Salivary secretion from rat submandibular gland (SMG) was induced by intravenous infusion into the femoral vein or partial perfusion of SMG with isotonic solution containing SP or autonomic stimulants. Blood and salivary flow rates, and electrolyte concentrations of saliva were measured. The relationship between electrolyte concentrations and salivary flow rate after intravenous infusion of SP was similar to that obtained using parasympathomimetic agents. Salivary flow rates induced by phenylephrine and isoproterenol were significantly increased by the further addition of SP, while the pilocarpine-induced flow rate was not affected. SP alone caused a significant increase in blood flow rate of perfused rat SMG. SP with atropine or phentolamine somewhat increased the blood flow. However, concomitant perfusion of atropine and phentolamine completely inhibited the SP effect. Salivary secretion induced by SP perfusion was reduced by atropine or phentolamine. Both blood flow elevation and salivary secretion induced by SP were reduced with increasing doses of a SP-antagonist. Also blood and salivary flow responses induced by phenylephrine were severely reduced by the SP-antagonist. On the other hand, the salivary secretion induced by pilocarpine was moderately reduced by the SP-antagonist. These results indicate that the salivation and especially the glandular vasodilation induced by SP were partially modified by the autonomic agents.

Animals↗
PubMed1989

Update on the management of glaucoma.

Most cases of chronic open-angle glaucoma can be treated medically. When medical management is ineffective, laser trabeculoplasty is usually performed. If medical management and laser treatment fail, surgery is the next step. Recently, ultrasound has been employed successfully for control of glaucoma when medical, laser, and surgical treatments were not successful. Acute angle-closure glaucoma is an ophthalmic emergency. This condition can be treated at an early stage by relieving the pupillary block with peripheral iridectomy by laser or surgery. Four major classes of drugs are currently used to treat glaucoma: carbonic anhydrase inhibitors, beta adrenergic blockers, parasympathomimetics, and sympathomimetics. Both local and systemic side effects may occur secondary to glaucoma medications and some of these may be severe or even fatal. These adverse reactions are discussed.

Glaucoma↗
PubMed1989

[Acute pandysautonomia and acute autonomic and sensory neuropathy].

Acute pandysautonomia and acute autonomic and sensory neuropathy were reviewed with special reference to their clinical entity, pathogenesis and clinical course. Since acute pandysautonomia was primarily described as an entity by Young et al. in 1969, a number of similar cases have been described. The disorder is characterized by severe sympathetic and parasympathetic impairment with relative or complete preservation of somatic motor and sensory functions. Some cases have only shown a cholinergic dysautonomia, while others have displayed a loss of autonomic function together with other impairments of nervous function. In 1980, Colan et al. reported a patient with acute autonomic and sensory neuropathy, manifesting severe sensory impairment and dysautonomia with marked loss of myelinated and unmyelinated fibers. Several other similar cases have appeared in the literature. Four years prior to the Colan et al. report, the author described a case which showed almost the same symptoms. At the present time, it is not clear whether this disorder is a new syndrome that is different from acute pandysautonomia or merely a subtype of it. The causes of the above two syndromes are unknown; however, an immunological disorder similar to the Guillain-Barré syndrome has been suggested. The clinical course is often protracted with slow improvement. However, from the author's experience, a relatively rapid improvement occurs after a single systemic administration of either parasympathomimetic or sympathomimetic agonists. Acute pandysautonomia which includes acute autonomic and sensory neuropathy has recently become more common: A number of similar cases have been reported worldwide, including many areas in Japan.

Acute Disease↗
PubMed1989

Neuropharmacology of the lower urinary tract in women.

One of the most common gynecologic complaints is urinary incontinence, which afflicts approximately one third of the female population. In urodynamic units, approximately 80 per cent of women with urinary incontinence have detrusor hyperreflexia as the sole reason for, or as a component of, their incontinence problem. Approximately 80 to 85 per cent of patients with detrusor hyperreflexia have a functional neuromuscular disturbance of their detrusor muscle. One to 2 per cent of the patients seen in our urodynamic unit have detrusor hyperreflexia caused by a neurogenic bladder. As our clinic's population ages, this type of functional neuromuscular disturbance--neurogenic bladder problem--will increase. The neuromuscular control of the lower urinary tract is complex and not fully understood, explaining why we are unable to treat the functional neuromuscular disturbance in some patients effectively and why we may have to try several drugs before finding one that is effective in other patients. Although patients may have the same symptoms and even the same urodynamic findings, the cause of the functional neuromuscular disturbance may be different. One patient may respond to drug A and not to drug B, and another patient with virtually the same symptoms and urodynamic findings responds to drug B and not to drug A. The main neurologic control of the lower urinary tract is through the sacral outflow of somatic and (mainly) parasympathetic nerve fibers. There appears to be an "on-off" control mechanism involving the urethrovesical unit wherein there is parasympathetic inhibition of the detrusor muscle and parasympathetic stimulation of the urethral smooth muscle and stimulation of somatic nerves to the urethral striated muscle at rest. Reverse action occurs when the patient voids. For this reason, cholinergic and anticholinergic drugs exert a powerful influence on the lower urinary tract. Adrenergic control through alpha 1- (and indirectly alpha 2-) and beta 2-receptors (with a preponderance of alpha-receptors in urethral smooth musculature and a preponderance of beta-receptors in the detrusor muscle) appears to modulate and modify parasympathetic action. This explains why adrenergic stimulant and blocker drugs, in most women, do not affect the lower urinary tract as much as parasympathomimetic-lytic drugs. However, adrenergic effect seems to be greater in some women than in others, explaining, for example, why some patients with detrusor hyperreflexia respond to beta 2-stimulatory drugs and not to anticholinergic drugs. Also inter-twined in the neuromuscular control of the lower urinary tract are the roles of prostaglandins and calcium-potassium channel changes.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗
PubMed1989

[Measurement of changes in parietal tonus of the abomasum in sheep].

An inflatable bag of 250 ml at the pressure of 2 mm Hg inside the abomasal lumen was used to identify the abomasal smooth muscle tone. Reduced tone of the ovine abomasum was assessed, like for the fundic part of the canine stomach, in relation with the cyclic motor activity of the proximal duodenum. Opposite effects were obtained following parasympathomimetic drug injection versus peptides of the gastrin group, suggesting a high responsiveness of the abomasal smooth muscle tone to both neural and hormonal influences.

Abomasum↗
PubMed1987

Angiotensin converting enzyme inhibitors in the clinic: first-dose hypotension.

A fall in blood pressure occurs, in most patients, within a few hours of a single dose of an angiotensin converting enzyme (ACE) inhibitor. While a serious fall in pressure is unusual in previously untreated essential hypertension, some patients are at risk of severe first-dose hypotension. These include those with treated heart failure, severe hypertension on polypharmacy, 'renin-dependent' renovascular hypertension and the occasional elderly patient. In such groups of patients the incidence of severe, symptomatic first-dose hypotension approaches 10%. This effect is not specific for ACE inhibitor therapy and may well occur as frequently with other drugs in such patients. First-dose hypotension may not be accompanied by tachycardia, possibly as a result of a parasympathomimetic action that may contribute to the first-dose effect. It is generally not possible to predict patients at risk, although plasma renin and angiotensin II concentrations show a modest positive correlation with the initial fall in blood pressure. The maximum initial hypotensive effect of ACE inhibitors is not clearly dose related but the duration of effect may be. Therefore such drugs should be started at minimum effective dosage. High-risk patients should be observed closely for at least 6 h. Symptomatic hypotension usually responds to supine rest although infusion of angiotensin II, atropine and occasionally saline may be required.

Atenolol↗
PubMed1978

[Therapy of alcoholism. The use of thiamine, ATP and magnesium and the control of clomethiazole sympathetic blockade (author's transl)].

Substitution therapy with thiamine, ATP and magnesium which, just like that with clomethiazole has a parasympathomimetic action, is based on the principle of suppression of the sympathetic system. If these patients are no longer capable for any reason of continuing to take the endogenous substances (thiamine, ATP and magnesium) by mouth, the treatment is continued with clomethiazole an an infusion. But since the intravenous administration of clomethiazole is not seldom accompanied by a parasympathetic coma with respiratory and cardiac depression and miosis, treatment of a sympathetic blockade with dextrose solution containing salt is proposed.

Adenosine Triphosphate↗
PubMed1988

[Effects of carbachol and atropine on bile secretion in sheep].

Experiments were performed on rams prepared surgically to make possible the control of bile flow and the maintenance of enterohepatic circulation of bile components. Carbachol and atropine were infused into the jugular vein for 2 hours in the amounts: 0.3 and 0.7 microgram/kg b.w./min. respectively. Carbachol administration did not affect significantly the bile production. Atropine led to the significant decrease in the bile flow (p less than 0.01) by diminished concentration of bile acids in the bile. On the basis of the obtained results the role of n. vagus in the regulation of biliary secretion is discussed. It is suggested, that in physiological conditions the biliary secretion is, to some extent, maintained as a result of the muscarinic receptor stimulation. This stimulation attains the maximum level and it is not possible to evoke rise in bile production after either n. vagus stimulation or administration of parasympathomimetic agents.

Animals↗
PubMedDate not supplied

Influence of castration and of the kind of sympathomimetic drug used upon the reactivity of rat seminal vesicles.

An interdependence of the hormonal state of rodents and the genital muscle response to drugs was observed either on females or on males. Castration or castration followed by oestradiol treatment increased the responses of rat seminal vesicles to parasympathomimetic drugs. As, however, the influence of such procedures upon the responses to sympathomimetic drugs is controversial, the parameters pD2 (apparent affinity constant), alpha (intrinsic activity) and rho (relative responsiveness) of adrenaline, noradrenaline, methoxamine and phenylephrine on the seminal vesicles isolated from normal and castrated rats were determined. These parameters were shown to be different, depending not only of the hormonal state of the donor animals, but also of the drugs tested on each preparation. These facts must be considered in studies about sensitivity of rat seminal vesicles to sympathomimetic drugs.

Animals↗
PubMed1977

Vasomotor reactions in the islets affecting the blood glucose levels.

1. The spiral nerve fiber and the nerve ganglion are demonstrated adjacent to the small pancreatic duct, artery and vein of the mouse in vivo. 2. Epinephrine and ephedrine, which are sympathomimetic amines, cause vasoconstriction of the afferent and efferent vessels of the islets of Langerhans and cause the interruption of circulation in the intrainsular capillary plexuses, which results in increased blood glucose levels. 3. Methacholine chloride, a parasympathomimetic drug, causes vasodilatation of the afferent and efferent vessels of the islets along with slower but continuous blood flow in the intrainsular capillary plexus, thus causes decreased blood glucose levels. 4. These changes in microcirculation of the islets of Langerhans in mice prove that one of the mechanisms of glucose homeostasis is mediated through autonomic nervous system by alteration of the vascular supply of the islets, which may be classified as neurovascular homeostatic regulator.

Animals↗
PubMed1978

[Clinical studies conducted with a new epinephrine derivative for the treatment of glaucoma (Dipivalyl epinephrine)].

Dipivalyl epinephrine, an epinephrine derivative, has been developed to improve the pharmacokinetic properties of the compound. Our open-label investigation included the administration of dipivalyl epinephrine ophthalmic solution to the eyes of 33 patients with an open-angle glaucoma. Former topical medication of parasympathomimetic agents was continued. The 0.1% dipivalyl epinephrine treatment approximated the results obtained with 1% epinephrine borate or phenylephrine 5% in reducing the intraocular pressure.

Clinical Trials as Topic↗
PubMed1987

[Diagnosis and therapy of mushroom poisoning (1)].

The diagnosis of mushroom poisoning is based on three principles: the description of the mushroom, the toxicological analysis of the mushroom and, most important, the mushroom syndrome. Mushroom poisoning can be classified according to the lag time between the meal and the onset of symptoms. In this paper we will discuss mushroom poisoning with short and intermediate lag time. With short lag time and a predominance of CNS signs and symptoms the diagnosis is either fly-agaric, pantherina or psilocybin syndrome. Parasympathomimetic signs and symptoms indicate the muscarine syndrome. If--with a lag period of up to four hours--vomiting and diarrhea are predominant, we will find a poisoning with one of the many mushrooms which lead to gastroenteritis. Gastroenteritis combined with hemolysis points to a paxillus syndrome.

Anemia, Hemolytic↗
PubMed1977

The pharmacology of N-carbamoyl-2-(2,6-dichlorophenyl)acetamidine hydrochloride (LON-954) a new tremorogenic agent.

The tremorogenic properties of a series of benzylimidoylurea derivatives are described. The most potent member, N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride (LON-954), produces a reproducible, dose-dependent rest tremor in the mouse with oral doses of 5-100 mg/kg which is also seen in other species (rat, cat, dog, rabbit). The tremor is of constant frequency, rapid onset and short duration. It is not accompanied by akinesia, muscle ridigity, antinociceptive activity, parasympathomimetic effects or marked hypothermia and in these respects differs from tremor produced by oxotremorine. Pretreatment with a microsomal enzyme inhibitor had no effect on the tremor. An LD50 of 165 mg/kg p.o. was calculated in the mouse. After repeated administration both acute and chronic tolerance developed to the tremorogenic effects of LON-954. Evidence for a central site of action is presented, since the tremor could be reproduced following injection of small quantities (50-100 microgram) into the cerebral ventricles of the mouse. Furthermore, the use of spinal, decorticate and and decerebrate rats indicated that although tremor is not of cortical origin, it arises in an area rostral to the inferior colliculi. The mechanism underlying the tremor appears to involve dopaminergic pathways, since the action of LON-954 was antagonised by L-dopa and apomorphine and potentiated by pimozide. Atropine and carbachol were without effect. It is suggested that LON-954 could be used as an alternative to oxotremorine for the detection of anti-Parkinson drugs, particularly those exerting their effects through dopaminergic mechanisms.

Analgesics↗
PubMed1981

[The effects of drugs on vesico-urethral function].

Disturbances of the bladder-urethra function may lead either to frequency, urinary incontinence, or urinary retention. A survey is given on the drugs most frequently used in the treatment of lower urinary tract dysfunction. Special attention is drawn to the use of parasympatholytics in the treatment of hyperactive detrusor function (unstable bladder), sympathomimetics in the treatment of decreased urethral resistance, parasympathomimetics in the treatment of hypoactive detrusor function and alpha-adrenergic blocking agents in the treatment of increased urethral resistance.

Adrenergic beta-Antagonists↗
PubMed1984

[The hypotensive effect of aromatic amidines and imidazolines].

Some amidine, diamidine and diimidazoline derivatives were tested on their ability to lower the blood pressure of the rat. Except for 5-amidino-2-phenylindole (271/179) all substances led to a short-lasting hypotension, the dose relationship of some of which was investigated. The biscationic character was a prerequisite for a strong hypotensive action. The predominantly peripheral origin of the blood pressure lowering action was shown for the substances pentamidine, diminazene, 6-amidino-2- (4-amidinophenyl)-indole (102/198), 5-amidino-2-(4-amidinophenyl) - benzofurane (150/49) and 2,6-diamidinoindole (261/115). A parasympathomimetic and histaminic efficiency could be excluded. The pressor effect of norepinephrine (noradrenaline) was reduced under the influence of pentamidine, diminacene and 102/198. With the dog 102/198 and 261/115 showed a diminution of heart rate and force as well as a vasodilatory effect. Using the rat, different cardiovascular parameters behaved analogous. Pentamidine, diminazene, 102/198 and 261/115 increased the force of contraction of the isolated rat atrium. Toxic effects were observed in doses as high as 0,5 mmol/l and l mmol/l. Pentamidine reduced the heart rate of the isolated atrium in a dose-dependent manner. Taking into account the in vitro results, the heart effects were interpreted as being reflectory. In the isolated rat aorta preparation the aforementioned substances in low doses shifted the dose-response curves of norepinephrine to the right, whereas higher doses also reduced the maximum contraction. Considering the results on the intact animal, a direct action of the diamidines on vascular smooth muscle was discussed.

Amidines↗
PubMed1983

Role of autonomic nervous system in the pathogenesis of angina pectoris.

The attacks of vasospastic angina or coronary spasm can be induced by injection of epinephrine, cold pressor test, Valsalva maneuver, and exercise. The attacks induced by these procedures can be suppressed by injection of phentolamine, an alpha adrenergic blocking agent in 80 per cent of the patients. On the other hand, propranolol, a beta adrenergic blocking agent, is not only ineffective in suppressing the attacks but aggravates the attacks in 50 per cent of the patients. Thus, alpha adrenergic receptors seem to play an important role in the production of vasospastic angina. The attacks of vasospastic angina can also be induced by injection of methacholine, a parasympathomimetic agent, and this reaction is suppressed by atropine, a parasympathetic blocking agent. Thus, parasympathetic nervous system also seems to play a role in the production of vasospastic angina. The attacks of vasospastic angina can be easily induced by adrenergic or parasympathetic stimuli from midnight to early morning but is usually not provoked by these stimuli in the daytime. Thus, there is circadian variation in the reactivity of coronary arteries to adrenergic or parasympathetic stimuli. There are also weekly, monthly and yearly variations of the reactivity of coronary arteries to these stimuli. Thus, alpha adrenergic or parasympathetic activity is not the sole factor in the production of vasospastic angina. Angina pectoris caused by increased myocardial oxygen demand is induced by infusion of isoproterenol, a beta adrenergic stimulant, and is suppressed by propranolol but not by phentolamine. So, beta adrenergic receptors play an important role in the production of angina pectoris caused by increased myocardial oxygen demand or organic angina pectoris.

Angina Pectoris↗
PubMed1983

Coronary arterial spasm in ischemic heart disease and its pathogenesis. A review.

Coronary arterial spasm plays an important role iun the production not only of variant angina but, also, of resting angina other than variant angina, of some exertional angina, and of some acute myocardial infarction. Coronary arterial spasm is most likely to occur at rest, particularly from midnight to early morning, and is usually not provoked by exercise in the daytime. This is related to the fact that the tone of coronary artery is increased from midnight to early morning, whereas it is decreased in the daytime after physical activities. Coronary arterial spasm can be induced by exercise, cold pressor test, hyperventilation, Valsalva maneuver, and the administration of pharmacological agents such as sympathomimetic agents (epinephrine, norepinephrine, etc.), beta-blocking agents (propranolol, etc.), parasympathomimetic agents (methacholine, pilocarpine, etc.), ergot alkaloids (ergonovine, ergotamine, etc.), alcohol, and others, particularly in the morning when spontaneous coronary arterial spasm is most likely to occur. Diltiazem and nifedipine, calcium-blocking agents, prevent coronary arterial spasm induced by these procedures in almost all patients. Phentolamine, an alpha-blocking agent, also suppresses coronary arterial spasm induced by these procedures in 81% of the patients. On the other hand, propranolol, a beta-blocking agent, is not only ineffective in suppressing coronary arterial spasm in 82% of the patients, but aggravates coronary arterial spasm in 41% of the patients. The acute attack of coronary arterial spasm can be promptly relieved by the administration of nitroglycerin.

Angina Pectoris, Variant↗
PubMed1984

Adie's syndrome: a medical treatment for symptomatic patients.

A symptomatic patient with Adie's syndrome is described as successfully managed with pilocarpine 0.125% applied topically to the involved eye three times daily. This is the first report of such a patient responding to direct parasympathomimetic therapy. Alternate approaches to the therapy of Adie's syndrome are mentioned. An approach to the management of Adie's syndrome is proposed.

Accommodation, Ocular↗