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We report a case of acute postcesarean colonic pseudo-obstruction (Ogilvie's syndrome). We report the treatment algorithm we followed. Recording to this algorithm may improve the treatment of this pathology and perhaps avoid surgical treatment in emergency.

Antiglaucomatous ocular side effects can be divided into specific and non specific ones. Non specific ocular side effects are mainly caused by preservative agents; they are essentially external ocular irritations. Specific ocular side effects are strongly related to the mechanism of action of the drug. These specific ocular side effects are described, caution being taken to precise the strength of the association between each side effect and the related drug by using the classification of World Health Organisation (WHO) (certain, probable, possible or unlikely).

Among the symptoms that may occur with smoking withdrawal, constipation is relatively frequent, but little studied.Three women reported that constipation developed when they stopped smoking and improved during transient relapses.This constipation sometimes produces serious functional disorders and can induce relapse. It occurs especially among women and those predisposed to it. Nicotine, by acting on the parasympathomimetic system, increases intestinal peristalsis, and a cigarette can appear to be effective self-medication. Magnesium salts are the first-line treatment for this problem. If they fail, neostigmine, an anticholinesterase with parasympathomimetic activity, appears remarkably effective in correcting this disorder.

[u]Buts[/u] : Etudier les effets des molécules anti-glaucomateuses couramment utilisées en pratique clinique aujourd’hui sur le nycthémère. [u]Méthodes[/u] : Revue de la littérature non exhaustive sur le sujet en utilisant les bases de données électroniques par recherche croisée sur les classes thérapeutiques antiglaucomateuses et les variations nycthémérales de la pression intraoculaire. [u]Résultats[/u] : L’efficacité d’une molécule sur la réduction de la pression intraoculaire pendant le nycthémère dépends de nombreux facteurs et demeure un champ encore mal connu. Les classes thérapeutiques les mieux explorées sont les bêtabloquants dont l’efficacité est diminuée la nuit et les prostaglandines qui part leur mode d’action original permettent de limiter les fluctuations circadiennes de la PIO. [u]Discussion[/u] : Des obstacles méthodologiques limitent notre savoir dans ce domaine car nous ne disposons pas encore d’un système d’enregistrement en continu de la PIO. Les antiglaucomateux ne sont pas équivalents en terme de réduction pressionnelle si l’on considère la pression intraoculaire sur 24 heures. [u]Conclusion[/u] : La chronobiologie et l’étude de l’effet des traitements anti-glaucomateux sont des sujets encore imparfaitement explorés, qui pourraient pourtant nous donner des clés pour le suivi de nos patients hypertones oculaires et glaucomateux à long terme.

Recent study showed that neostigmine (500 microg) by intra-articular produces postoperative analgesia without adverse effect. The author's goal was to determine whether 500 microg of neostigmine added to bupivacaine in axillary plexus block could prolonged postoperative analgesia without increasing the incidence of side effects.Ninety patients scheduled for orthopedic or plastic surgery with axillary plexus block were randomly assigned to one of 3 groups : group 1 (TGr n = 30) received saline solution (1 ml) in the axillary plexus, group 2 (NAGr n = 30) received 500 microg (1 ml) neostigmine in the axillary plexus and group 3.500 microg neostigmine subcutaneously (NSGr n = 30). We evaluated visual analog pain scores (VAS), the consumption of the ketoprofene, nausea and vomiting incidence during the first 24 h. ANOVA, Kruskall Wallis and Fisher tests were used for statistical analysis. A p value of0.05 was considered significant.The VAS score was lower in NAGr (21 +/- 18) vs NSGr (31 +/- 14) and control group TGr (45 +/- 2) (p0.05). The consumption of the ketoprofene is 127 +/- 65 mg in NAGr vs 150 +/- 53 mg in NSGr and 200 +/- 50 mg in group TGr (p = 0.02). Incidence of nausea and vomiting was 3.5% in NAGr vs 6.8% in NSGr and 0% for TGr.Neostigmine combined to a mixture of lidocaine and bupivacaine prolongs postoperative analgesia after axillary plexus block.

The rationale for the use of muscarinic antagonists in bronchopulmonary dysplasia (BPD) is based on the physiology and pharmacology of airway smooth muscle, the pathology of BPD, and the response of infants with BPD to bronchodilators, in vivo and in vitro studies of airway smooth muscle of newborn animals and humans indicate that vagal efferent airway innervation and/or muscarinic receptors are functional at birth, as well as early in gestation. Current concepts regarding muscarinic receptor subtypes suggest that M3 receptors mediate airway smooth muscle contraction, M2 receptors are autoinhibitory and limit vagally-mediated bronchoconstriction, and M1 receptors may play a facilitatory role in ganglionic transmission. Muscarinic receptor subtypes appear to be functionally expressed at birth but may undergo developmental regulation. Infants with BPD have an elevated pulmonary resistance that is accompanied by hypertrophy of airway smooth muscle, b2-agonists cause bronchodilation in BPD as does atropine in infants recovering from severe BPD. The synthetic congener of atropine, ipratropium bromide (IPB) causes bronchodilation in ventilator-dependent infants with BPD in a dose-dependent fashion. Nebulized IPB causes a decrease in respiratory resistance that reaches a maximum of 20% at 175 mg. The bronchodilation seen with muscarinic antagonists suggests that part of the elevated resistance associated with BPD is due to increased muscarinic tone, presumably vagal in origin. When IPB is combined with salbutamol (0.04 mg) the response is increased in magnitude and duration; reaching a slightly larger decreases in resistance (26%) that is now accompanied by an increase in compliance (20%).(ABSTRACT TRUNCATED AT 250 WORDS)

After reviewing the nervous control of the lower urinary tract, the author defines the action of various drugs on the bladder, bladder neck, urethra (smooth and striated sphincter). The drugs are classified according to their stimulant or blocking effect on the sympathetic and parasympathetic nervous systems and alpha and betadrenergic receptors. Drugs acting on smooth and striated muscle fibres are then studied and the iatrogenic adverse effects of these drugs are mentioned.

The evaluation of neurogenic vesicosphincteric disorders is based on clinical examination and instrumental assessment, composed of urodynamic and perineal electrophysiological studies allowing a better understanding of the pathophysiology, aetiopathogenesis and course of the symptoms. The treatment of urinary symptoms, whether medical, surgical, mixed or involving various rehabilitation techniques, must satisfy a dual objective of individual and psychosocial comfort and preservation of the patient's uronephrological future.

As well as being present in all mammals, yawning occurs, at least in its mandibular component, in all vertebrates. The existence of pathological and pharmacologically induced yawning justifies study of this everyday ENT reflex. Its mechanism remains uncertain. The most likely hypothesis would seem to be stimulation of the reticular system of the brain-stem by signals originating in masseteric neuromuscular spindles sensitive to stretching. Serotoninergic inhibition from the dorsal raphe, a fall in hypothalamic dopaminergic inhibitory tone, followed by ocytocinergic hippocampal activation and then more diffuse cholinergic activation of cranial nerve motor nuclei seems likely. Various hormonal or socio-environmental influences can modify the activity of these different systems. The physiological consequences and the communicative value of yawning become more diversified with the phylogenetic evolution of the subject. Yawning appears to correspond to an alertness reflex which has acquired a paralinguistic value with evolution and may have a role in protection or social cohesion.

Malakoplakia is a fairly rare disease, normally found in women (four out of every five cases). It mainly attacks the urinary system, but may spread to the other viscera. The symptoms are not clinically specific. The main interest of the disease is its pathogenesis, from which its treatment is derived. It is in fact an immunological dysfunction of the phagocytes, leading to chemical disorders in the macrophages. Its treatment is based on the use of cholinergic agonists and vitamin C therapy.

Because it intervenes in normal and pathological cerebral ageing, plays a role in late dyskinesias of Parkinson's syndrome and is involved in the memorization processes, central cholinergic neurotransmission deserves to be known with precision. Its physiological approach deals with the anatomical organization of the central cholinergic system and with the mechanisms of synthesis, release and degradation of acetylcholine and its interaction with its receptors. The pharmacological changes (inhibition or stimulation) conceivable at different levels lead to therapeutic applications.

The investigation of 3 day old notochords by the fluorescence method of Falck and Owman showed an increase of the fluorescence after treatment of the chick embryos at 48 hrs of incubation, with nicotine sulfate or carbachol. The addition of norepinephrine or L-Dopa emphasized the formaldehyde induced fluorescence. The simultaneous treatment with a cholinergic agent and atropine, propranolol or reserpine decreased or suppressed the fluorescence. These results demonstrate the existence of a relationship between the treatment with a cholinergic agent and the amount of chordal biogenic amines.

Stopped-flow studies of receptor-rich membrane fragments from Torpedo marmorata labelled by quinacrine lead to the resolution (in the time scale of the millisecond to the second) of a fast increase of fluorescence intensity associated with the binding of typical agonists. The signal is reversible, does not take place with antagonists, has a Q10 of 1.4 and its amplitude decreases after pretreatment of the membrane fragment by dithiothreitol or ceruleotoxin.

Regression of Urrets-Zavalia's syndrome was obtained in one case after treatment administered according to a strict sequence following keratoplasty for keratoconus: sympatholytic drops (guanethidine 5%-Ismelin) every 4 hours for 24 hours, followed the next day, when mydriasis had been slightly reduced, by parasympathomimetic drops (pilocarpine 2%). Marked myosis was observed and treatment discontinued. This resulted in recurrence of the mydriasis, but this was successfully treated by repeating therapy. Pilocarpine drops were progressively diminished, followed by a slow reduction of guanethidine drops over 8 weeks, resulting in only slight residual anisocoria. This treatment is based on the physiopathological concept of sympathetic spasm with parasympathetic inhibition, and it is suggested that reduction of spasm should be obtained before administration of therapy to stimulate the sphincter. Pharmacological data on the compounds employed are discussed.

Muco-ciliary transport is only effective because of the coordination of the ciliary beats (metachronous) and the harmony between mucus and cilia. The tip of the cilia is in contact with a jellyform layer of mucus propelled to the oropharynx. This jellyform layer has a complex rheological behaviour: it flows like a liquid and shapes like solid elastic. When the rheological properties of bronchial secretion are abnormal, mucociliary transport becomes inefficient. However, the most fluid secretions are not necessarily best transported, because the elasticity and viscosity to guarantee efficient muco-ciliary transport can only vary within defined limits. The mechanism regulating the ciliary beats is poorly understood; the bronchial secretions conduct impulses through the autonomic nervous system as well as mediators such as histamine and the metabolites of arachidonic acid. Mucociliary function may be studied either, directly through mucociliary transport or through mucociliary clearance. A fall in mucociliary activity can be produced by a primary ciliary disorder, by bronchial disease or the consequences of respiratory infection. General anaesthetics and Atropine slow mucociliary transport but Ipratropium bromide does not; Theophylline and sympathomimetics speed it up. The expectorants are mucolytics (proteolytic enzymes, N-acetyl-cysteine), there are agents to correct hydration anomalies of the bronchial secretion (water, hypertonic sodium chloride) iodides, antifibrins by substitution, anti-inflammatory agents and mucoregulatory agents (S-carboxymethylcysteine, bromhexine). The efficacy of the greater part of these expectorants has not been established in vivo by controlled therapeutic trials.

The injection of certain cholinergic agents in the yolk sac of young Chick embryos (40 to 48 hrs. of incubation) gives rise to a twisting of the cervical notochord and spinal cord and contraction of the cervical somites. These morphogenetic changes result in spinal column malformations in older embryos. The effects of the cholinergic agents are inhibited by simultaneous treatments with a cholinergic agonist and an antagonist or a cholinergic receptor ligand. The results lead to the assumption that the early embryos already possess cholinergic receptors, probably located in the notochord.

Drugs induced respiratory disorders include bronchospasm, extrinsic alveolitis, and diffuse interstitial pulmonary fibrosis. Bronchospasm may be due to the action of pharmacodynamic agents on autonomic control of bronchial tone (beta-blockers, beta-agonists...) or to a hypersensitivity reaction (penicillins, sulfonamides, anti-inflammatory compounds...). Extrinsic alveolitis usually follows administration of anti-infective medication but other drugs may be implicated. Prolonged use of a wide variety of drugs, particularly cytotoxic agents, is necessary to provoke the onset of a diffuse interstitial pulmonary fibrosis.

This review deals successively with the anatomy and physiology of cardiac autonomous control, the mechanisms underlying the arrhythmogenic effects of the parasympathetic and sympathetic systems and the role played in their therapeutical effects by the interaction between antiarrhythmic durgs and the autonomous control of the heart.

The analysis by stopped-flow of the interaction of fluorescent agonist (C5DACho1) with the acetylcholine receptor in its membrane-bound form reveals several kinetic steps: a fast one, in the millisecond range, associated with the binding of C5DACho1 to a high affinity state and a "medium" and "slow" one, the last one representing possibly an isomerisation of the receptor molecule towards the high affinity state.

Pulmonary surfactant is a lipoprotein made up mostly of tensio-active phospholipids. It is synthesized by type II pneumocytes and accumulates as lamellar bodies before being excreted into pulmonary alveoli where it fills intercellular spaces and results in a liquid film (about 1 micron thick) covering the alveolar wall. Surfactant turnover occurs through the action of phospholipases from the alveolus or pneumocytes. Level of alveolar surfactant dependents on the ratio of synthesis and degradation of its principal constituent, dipalmitoyl-phosphatidylcholine. Many substances are known to be able of alter this ratio. Among these, synthetic glucocorticosteroids appear to be the most active in increasing alveolar surfactant. The multiple possible sites of action of these steroids explain their relative efficacy in the prevention of respiratory distress in humans. Studies in progress should increase the number and the quality of drugs available for this purpose.

Two technics (chronic electrodes-electrointraperitoneography : EIG) have been used simultaneously in the conscious dog for the pharmacological study of drug effects on the electrical activity of intestine. The results show a good correlation between records obtained with the technic which needs a surgical operation (chronic electrodes) and the other which doesn't (EIG). The expected effects of the parasympathomimetic (acetylcholine-neostigmine) parasympatholytic (scopolamine) and adrenergic (epinephrine-neosynephrine) drugs used on the spiking activity are obtained with the two technics.

In relation to two cases of paradoxal systemic reaction following instillation of pilocarpine and acetylcholine, we discuss risk factors which promote these reactions and propose an etio-pathogenical hypothesis. Furthermore, as one of the patients presented also a hypersensitivity to epinephrine; he associated two manifestations which, to our knowledge, have not yet been reported in the same patient.