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At least 541 records · Page 30Linked to original sources
PubMed1990

Action of pinaverium bromide, a calcium-antagonist, on gastrointestinal motility disorders.

1. The evidence reviewed here indicates that pinaverium bromide (Dicetel) relaxes gastrointestinal (GI) structures primarily by inhibiting Ca2+ influx through potential-dependent channels of surface membranes of smooth muscle cells. 2. The in vivo selectivity of pinaverium bromide for the GI tract appears to be due mainly to its pharmacokinetic properties. Because of its low absorption (typical for quaternary ammonium compounds) and marked hepatobiliary excretion, most of the orally-administered dose of pinaverium bromide remains in the GI tract. 3. Orally-administered pinaverium bromide does not elicit adverse cardiovascular side-effects at doses that effectively relieve GI spasm, pain, transit disturbances and other symptoms related to motility disorders. 4. Pinaverium bromide is the only Ca2(+)-antagonist with known therapeutic efficacy in the treatment of irritable bowel syndrome and certain other functional intestinal disorders.

Animals↗
PubMed1996

Gastrointestinal motility in the neonate.

Many aspects of the forward propulsion of enteral nutrients are not fully mature in the preterm and term neonate. Because the regulation of motor activity in the gastrointestinal tract is complex and multifaceted, many levels of regulation of this activity are immature in the preterm infant; however, as neonatologists develop a better understanding of the physiologic mechanisms that underlie these dysfunctions as well as the interactions of nutrients, hormones, and pharmacologic agents with these regulatory mechanisms, better feeding strategies can be tailored for these infants. Moreover, current studies will permit the development of predictive and diagnostic tools as well as the refinement of pharmacologic interventions for these infants.

Feeding Behavior↗
PubMed1993

Origin and control of gastrointestinal motility.

As a result of improved understanding of the origin and control of motility at both the whole organ and the cellular level, a scientific approach to the diagnosis and treatment (both medical and surgical) of motility disorders has evolved. Examples are present for all levels of the gastrointestinal tract. Manometric, myoelectric, and pharmacologic studies have elucidated the role of the lower esophageal sphincter and stomach in the pathogenesis of gastroesophageal reflux and determined the mechanism of successful medical and surgical treatment. Better evaluation of colorectal motility using colonic transit studies, pelvic floor radiography, and rectoanal manometrics has led to a better identification of both the etiology of severe constipation and patients who will have a successful surgical outcome. Studies of normal and abnormal gallbladder motility and responsiveness to hormonal stimulation have shed light on the cellular abnormalities in gallbladder myocytes that predispose to gallstone formation. Finally, since we have learned that certain surgical procedures affect motility in an adverse manner, a better basic understanding of gastrointestinal physiology has led to a better clinical understanding of the mechanism by which the changes occur and to the development of more directed physiologic operations. The classic example is seen in ulcer surgery, where the introduction of highly selective vagotomy instead of truncal vagotomy preserved antral innervation and decreased the incidence of postvagotomy complications. All these concepts and more are addressed in more detail in subsequent articles in this issue.

Animals↗
PubMed1985

Peripheral receptor populations involved in the regulation of gastrointestinal motility and the pharmacological actions of metoclopramide-like drugs.

This minireview is concerned with a re-examination of the locus of action and the possible peripheral mechanisms involved in the gastrointestinal (GI) stimulant effects of metoclopramide. Such a re-evaluation is opportune given the increasing use of this drug in the therapy of certain GI tract disorders. To provide an orientation on this subject the location in the GI tract and function of several relevant receptor types have been reviewed. In the past metoclopramide has been reported to enhance contractions of a variety of GI preparations to electrical stimulation, acetylcholine, carbachol and ganglion stimulants, to inhibit responses to alpha 2-adrenoreceptor agonists and 5-hydroxytryptamine, as well as blocking those to dopamine. Also in such preparations metoclopramide facilitates the release of acetylcholine to transmural stimulation. One important question is whether this effect is mediated via a specific prejunctional receptor. In this respect 2 suggestions have been made. Firstly that the drug may act as a preferential, prejunctional muscarinic antagonist thus inhibiting the negative feedback inhibition of acetylcholine release and secondly that metoclopramide may be a prejunctional agonist (partial) at 5-hydroxy-tryptamine receptors. Although the latter possibility appears most tenable at present, the involvement of a specific receptor remains to be confirmed. The important finding that dopamine receptors are probably not involved in the local stimulant effects of metoclopramide has important implications for future research orientated towards the discovery of a new generation of GI drugs lacking the side effects associated with central dopamine receptor blockade. Several compounds (cinitapride, BRL 20627A and cisapride) are now in the early stages of clinical evaluation.

Animals↗