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At least 1,495 records · Page 83Linked to original sources
PubMed1992

General pharmacology of the new quinolone antibacterial agent levofloxacin.

The general pharmacological properties of (-)-(S)-9-fluoro-2,3-dihydro-3- methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido[1,2,3-de][1,4] benzoxazine-6-carboxylic acid hemihydrate (levofloxacin, DR-3355, CAS 100986-85-4), an optically active isomer of ofloxacin, were examined. 1. Central nervous system (CNS): DR-3355 at 200-600 mg/kg p.o. showed depressant activity on the CNS, as was indicated by the depressant syndrome (mice), decreased spontaneous motor activity (mice) and hypothermia (mice and rabbits). In the cat behavior and EEG experiments, it had both stimulant and depressant effects at 30-100 mg/kg i.p., and caused transient slow waves followed by seizures at 20-30 mg/kg i.v. DR-3355 had no effect on convulsion, hexobarbital anesthesia, pain reaction to a tail pinch, or conditioned avoidance response, except that it showed mild analgesic activity in acetic acid writhing at 600 mg/kg p.o. 2. Respiratory and cardiovascular system: DR-3355 produced a hypotensive and a bradycardiac effect after the rapid i.v. injection of 6 mg/kg or more in anesthetized dogs, accompanied by an increase in plasma histamine concentration. Both changes were markedly reduced when the test drug was administered by continuous i.v. infusion. 3. Autonomic nervous system: DR-3355 inhibited nictitating membrane contraction induced by both pre- and post-ganglionic stimulation, and inhibited the depressor response to acetylcholine at 20 mg/kg i.v. It had no influence on pupil size or on pressor response to norepinephrine. 4. Gastrointestinal system: DR-3355 at 600 mg/kg p.o. inhibited gastric secretion. Dog gastrointestinal motility was slightly inhibited, and was then stimulated over the dose range of 2-20 mg/kg i.v. It had no influence on gastrointestinal propulsion, the gastric emptying rate or the gastric mucosa. 5. Isolated smooth muscle: At a concentration of 5 x 10(-4) g/ml, DR-3355 was devoid of spasmogenic or smasmolytic activity, except for showing a slight relaxation effect (trachea), inhibition of nicotine-induced contraction (ileum) and spontaneous or oxytocin-induced motility (pregnant uterus). 6. Miscellaneous: DR-3355 inhibited the urine output and carrageenin-induced paw edema at 600 mg/kg p.o. It had no effect on skeletal muscle contraction or the corneal reflex.

Animals↗
PubMed1992

Endogenous CCK is not involved in the regulation of interdigestive gastrointestinal and gallbladder motility in conscious dogs.

In this study, we assessed whether endogenous CCK is involved in the regulation of interdigestive gastrointestinal and gallbladder motility in conscious dogs with force transducers chronically implanted in the gastric antrum, duodenum, jejunum and gallbladder. L364718 at a dose of 1.0 mg/kg was used as a specific and potent CCK receptor blocker, and its effect on spontaneous interdigestive motility and plasma motilin release were examined. Additionally, the contractile activity of exogenous synthetic canine motilin (20-100 ng/kg) with or without pretreatment with L364718 at a dose of 1.0 mg/kg was assessed. Whether the blocking effect of L364718 on CCK receptors was sufficient or not was verified by giving CCK-OP at a bolus dose of 10 ng/kg. As a result, cyclic changes in interdigestive motor activity and the plasma motilin concentration were not affected by pretreatment with L364718. L364718 also did not affect motilin-induced interdigestive contractile activity in the gastrointestinal tract and gallbladder. On the other hand, the effect of CCK-OP was completely abolished by pretreatment with L364718. It is concluded that endogenous CCK is not involved in the regulation of spontaneous and motilin-induced interdigestive contractions in the canine gastrointestinal tract and gallbladder.

Animals↗
PubMed1999

Age-induced changes in the enteric nervous system in the mouse.

The enteric nervous system of the murine gut was investigated by immunocytochemistry in 1-, 3-, 12- and 24-month-old mice, using protein gene product 9.5, a general marker for nerve elements. Myenteric and submucosal plexi were quantified by computerized image analysis. In antrum, there were significantly fewer neurones per ganglion in both myenteric and submucosal ganglia of 12- and 24-month-old mice than in 3-month-old animals. The same was true of duodenum and colon. The relative volume density of nerve fibres in antral muscularis propria was significantly greater in the 1-, 12- and 24-month-old mice than in the 3-month-old mice. In colon, there were fewer submucosal ganglia per millimetre baseline in 1-month-old mice than in 3-month-old mice. The colonic myenteric ganglion in 1-, 12- and 24-month-old mice was smaller than in 3-month-old mice. There was no statistical difference between females and males regarding the number of ganglia per millimetre baseline, ganglionic area, number of neurones per ganglion or the relative volume density of nerve fibres in either the myenteric or submucosal plexi. As the enteric nervous system is responsible for coordinating and integrating the motility of the gut, the ageing-related changes reported here may well be of some relevance for the increased gastrointestinal motility dysfunction in the elderly persons.

Aging↗
PubMed2000

Reflux in children.

Gastro-oesophageal reflux (GOR) is an extremely common paediatric problem that often runs a harmless and self-limited course. Physiological GOR however can lead to marked parental anxiety, many unnecessary investigations and often unwarranted and potentially harmful therapeutic interventions. Our ability to better define GOR and gastro-oesophageal reflux disease (GORD) has improved in the past 15 years with a better understanding of the pathophysiology in infants and children due to the development and wider use of flexible endoscopy, 24-hour oesophageal pH monitoring and, more recently, the use of micromanometric methods for studying oesophageal motility. This will be further enhanced in the future with the development of non-invasive breath testing to study gastrointestinal motility and the use of electrical impedance to study fluid movement. Our therapeutic interventions have also improved particularly in the areas of acid suppression, improved surgical techniques and most recently laparoscopic fundoplication. This chapter reviews these advances in the paediatric area especially with regard to pathophysiology, diagnostic testing and therapeutic intervention.

Age Factors↗
PubMed1992

Irritable bowel syndrome.

The irritable bowel syndrome is a common disorder of gastrointestinal motility. Abdominal pain, bloating, and inconsistent bowel habits are the hallmark symptoms of irritable bowel syndrome. Fever, weight loss, and gastrointestinal bleeding often indicate more serious pathologic gastrointestinal conditions, such as inflammatory bowel disease or infectious enteritis. Because irritable bowel syndrome is so prevalent in our society, the primary care physician should be able to readily recognize the clinical features of this disorder in order to spare patients expensive, unnecessary diagnostic and therapeutic interventions. In this review, the authors discuss the clinical and psychological features of irritable bowel syndrome and offer a useful approach to the diagnosis and treatment of this disorder.

Colonic Diseases, Functional↗
PubMed1992

The role of the gastrointestinal tract in the development of burn sepsis.

Conceptualization of the gastrointestinal tract as the "motor" that drives sepsis and multiple-system organ failure has only recently been appreciated. Most of the investigation into the pathophysiology of gut-derived sepsis involves using animal models; however, some of the findings are already being corroborated in human studies. The gastrointestinal tract is a dynamic organ whose function as a front-line defense against infection needs to be appreciated. The development of lethal sepsis is a function of the microbial load and virulence, the status of the gastrointestinal barrier, and the magnitude of the host defense response. In assuming care of a critically ill patient, we must be judicious in the use of antibiotics in order to prevent intestinal overgrowth of potential pathogens. Providing proper nutrition by an enteral route (when possible) not only satisfies caloric needs but regulates the microflora and maintains the integrity of the mucosal barrier. Burn patients should receive enteral nutrition early, the first day if possible. This not only will protect the intestinal mucosa but also will blunt the hypermetabolic response following thermal injury. Lastly, the patient should not receive an excessive amount of narcotic or sedative, for these drugs have an inhibitory effect on gastrointestinal motility, encouraging bacterial overgrowth. In the near future, new therapeutic modalities may soon become available to protect and treat the compromised gastrointestinal barrier. These modalities may include, but certainly are not limited to, the use of glutamine and xanthine oxidase inhibitors to prevent stress-related injury to the gastrointestinal mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Functional gastrointestinal disorders and mast cells: implications for therapy.

The pathophysiology of functional gastrointestinal disorders is poorly understood. Accepted common mechanisms include psychosocial factors, abnormal gastrointestinal motility and disturbed visceral sensory perception, but the underlying causes remain unclear. Mast cells (MCs) are immunocytes widely distributed throughout the gastrointestinal tract. Several stimuli (e.g. allergens, neuropeptides and stress) lead to MC activation with consequent mediator release (e.g. histamine, tryptase and prostanoids). The MC mediators interact with nerves supplying the gut leading to altered gut physiology and increased sensory perception. The intestinal mucosa of irritable bowel syndrome patients contains on average an increased number of MCs. These cells release an increased amount of mediators in close vicinity to mucosal innervation. The MC activation and their close proximity to nerve fibres is correlated with the severity of perceived abdominal painful sensations. These data provide a strong basis for considering MCs as important participants in visceral hypersensitivity and pain perception in irritable bowel syndrome. Inhibition of MC function may ameliorate irritable bowel symptoms. Novel drugs with an increased potential in the control of MC function (e.g., anti-IgE antibodies, the intracellular protein tyrosine kinase inhibitor Syk) and mediator release (e.g., second generation antihistamines, proteinase-activated receptor antagonists) may be useful pharmacological tools for these common disorders.

Animals↗
PubMed2003

Endogenous gamma-hydroxybutyric acid is in the rat, mouse and human gastrointestinal tract.

By using Gas Chromatography-Mass Spectrometry high concentrations of endogenous gamma-hydroxybutyric acid (GHB) have been demonstrated in the rat and mouse gastrointestinal tract, including stomach, small intestine and colon-rectum. GHB concentrations were many folds higher than those present in the brain. High GHB concentrations have been also found in the human operatory specimen of sigmoid colon. Since GHB administration has been found to modify gastrointestinal motility via GABA(B) receptors, the present results suggest that endogenous GHB might be involved in the GABA(B) receptor-mediated control of gastrointestinal function.

3-Hydroxybutyric Acid↗
PubMed1995

Otenzepad shows two populations of binding sites in human gastric smooth muscle.

Cholinergic agonists and antagonists frequently used for gastrointestinal motility disorders often produce adverse effects. A possible explanation for this is the presence of similar muscarinic receptor subtypes on smooth muscle from different gastrointestinal organs. The aim of this study was to characterize muscarinic receptor subtypes in human gastric smooth muscle with receptor binding methods. N-[3H]Methylscopolamine ([3H]NMS) saturation experiments showed a homogeneous population of noninteracting binding sites (KD = 0.76 +/- 0.07 nM, Bmax = 46.94 +/- 3.69 fmol/mg of tissue protein, nH = 0.99 +/- 0.01). The rank order of inhibition of [3H]NMS binding by nonlabelled compounds was atropine >> otenzepad >> pirenzepine. Atropine and pirenzepine bound to a homogeneous population of binding sites. The inhibition of [3H]NMS binding by otenzepad showed two populations of receptors (nH < 1, p < 0.01), whose apparent Ki1 of 298 +/- 40 nM and apparent Ki2 of 3.463 +/- 0.62 mM were similar to those reported for the M2 and M3 muscarinic receptor subtypes. The M2 subtype was the more abundant of the two, representing 79.12 +/- 5.48% of the total population. We conclude that two muscarinic receptor subpopulations similar to the M2 and M3 subtypes are present in human gastric smooth muscle and that the M2-like receptor is the more abundant of the two.

Adult↗
PubMed2002

Effects of progesterone on gastric emptying and intestinal transit in male rats.

AIM: To study the dose-dependent of progesterone (P) effect and the interaction between the oxytocin (OT) and P on gastrointestinal motility. METHODS: In order to monitor the gastric emptying and intestinal transit, the SD male rats were intubated via a catheter with normal saline (3 ml/kg) containing Na(2)(51)CrO(4) (0.5 microCi/ml) and 10% charcoal. OT was dissolved into normal saline and P was dissolved into 75% alcohol. RESULTS: Low does of P (1 mg/kg, i.p.) enhanced the gastric emptying (75+/-3%, P<0.05) and high dose of P (5 mg/kg, i.p.) inhibit it (42+/-11.2%, P<0.01). P (1 mg/kg) increased the intestinal transit (4.2+/-0.3, P<0.05) while the higher dose (10-20 mg/kg) had no effect. OT (0.8 mg/kg, i.p.) inhibited the gastric emptying (23.5+/-9.8%, P<0.01). The inhibitory effects of P(20 mg/kg) (32+/-9.7%, P<0.05) and OT (0.8 mg/kg) on gastric emptying enhanced each other when the two chemicals were administrated simultaneously (17+/-9.4%, P<0.01). CONCLUSION: Low dose of P increased GI motility while high dose of P decreased it. During the later period of pregnancy, elevated plasma level of OT may also participate in the gastrointestinal inhibition.

Animals↗
PubMed2006

Functional dyspepsia--a multicausal disease and its therapy.

Functional dyspepsia is a common chronic disorder with non-specific upper abdominal symptoms which can not be explained by organic or biochemical abnormalities. The dyspeptic symptoms are very compromising and bothersome and result in a substantial reduction of quality of life. The substantial direct and indirect medical and economical costs induce a high socioeconomic interest in the pathogenesis and the treatment options of this disease. Over the past 30 years several theories about the etiology of the symptoms in functional dyspepsia patients have been put forward. These include disorders of gastrointestinal motility, acid secretion, visceral hypersensitivity, adaptation and accommodation, Hp-infection, mucosal inflammation and finally genetic predisposition. There is increasing evidence that functional dyspepsia is a multi-causal disorder, which leads to altered processing of afferent information from the gastrointestinal tract to the CNS. Autonomic hypersensitivity and altered central processing could be a common phenomenon whereas motility changes, inflammation or altered secretion could increase neural afferent inputs. Treatment of this complex disorder could and should involve these different levels of symptom generation. Thus different approaches with anti-secretory, spasmolytic, prokinetic and anti-inflammatory effects and most preferably reduction of visceral hypersensitivity seem logical. This could explain the variety of drugs which show a positive symptomatic response. This could also offer the conclusion, whether a combination of these drugs could be clinically superior which remains to be proven. And this could offer a logical approach for the use of substances with a multi-target action, e.g. STW 5.

Diagnosis, Differential↗
PubMed1995

Chronic intestinal pseudo-obstruction in childhood: progress in diagnosis and treatment.

Chronic intestinal pseudo-obstruction is a clinical diagnosis based on signs and symptoms of bowel obstruction in the absence of a physical obstruction demonstrable by X-ray or surgery. The phenotype may be caused by gastrointestinal motor, sensory, or psychological disturbances, or even by Munchausen's syndrome-by-proxy. Interactions between these pathophysiologic mechanisms may result in changes in the clinical presentation during development, including an increase in the number of affected children complaining of chronic abdominal pain. Chronic pain or the fear of pain may cause children to limit their voluntary oral intake, necessitating tube or parenteral supplements. A multidisciplinary team approach which includes input from the pediatric gastroenterologist, pain management specialist, and psychologist is most likely to effect positive change. In considering a diagnosis of chronic intestinal pseudo-obstruction, the clinician is obligated to evaluate gastrointestinal motility and sensory function, as well as the behavior of the child and family. This review aims to provide a biopsychosocial conceptual framework for understanding the heterogeneous group of gastrointestinal neuromuscular conditions that are diagnosed as chronic intestinal pseudo-obstruction. It will also provide a review and critique of the utility of new diagnostic methods, including antroduodenal and colonic manometry, and new therapeutic options, including the prokinetic agents such as cisapride which increase motility, and intestinal transplantation.

Child↗
PubMed1998

[Modulatory mechanisms involved in the parasympathetic excitatory neuro-effector transmission in the airway and gastrointestinal tracts--perspective for a new drug creation].

It is generally considered that dominant excitatory control of airway and gastrointestinal tract is exerted by the parasympathetic nervous system, and the transmitter output from the nerve terminals, mainly acetylcholine (ACh), is modulated in many ways for example by ACh itself, prostaglandins E series (PGE) neuropeptides and nitric oxide (NO). These modulations are probably due to the suppression of high-voltage-activated calcium channels in the nerve terminals, since, for example, ACh or prostaglandin E1 & E2 selectively suppressed both the N- and R-type Ca2+ currents, through M2 muscarinic and EP3-receptors, respectively in paratracheal ganglion cells. Parasympathetic nervous system also releases nonadrenergic-noncholinergic (NANC) inhibitory neurotransmitters in addition to ACh. The threshold level for ACh and NO release, for example, is almost identical, thereby suggesting the possible interactions between NO and ACh at the post-junctional cites, in addition to the prejunctional inhibitory action of NO to suppress ACh release from the nerve terminal. In this context, NO-donors, including SNAP or Cys-NO, reduced the amplitude of carbachol-induced Ca(2+)-dependent Cl- currents (I infinity h, I alpha(Ca)) dose-dependently (IC50: about 10 microM) in the cat tracheal myocytes, and similar inhibition was also exerted by dibutyryl cGMP (db-cGMP). However, two structurally distinct types of G-kinase inhibitor, H-8 (2.5 microM) and KT5823 (1 microM) failed to counteract the inhibitory effects of SNAP or db-cGMP. Another G-kinase-specific inhibitor, (Rp)-8-pCPT-cGMPS, itself caused a marked reduction in I infinity h, thereby indicating that inhibition of I infinity h by NO donors involves a cGMP-dependent but G-kinase-independent mechanism. All these experimental facts taken together indicate that there are pre- and post-junctional "brakings" in the excitatory parasympathetic neuro-effector transmission. Furthermore, in the gastrointestinal tract, Z-338, a newly synthetized gastroprokinetic agent, stimulates gastrointestinal motility through inhibition of the pre-junctional braking system through inhibition of M1 receptors. Such a drug may be useful to control the respiratory and gastrointestinal smooth muscles.

Animals↗
PubMed1988

[The agonist-antagonist nalbuphine prolongs gastro-cecal transit time and induces short-term pain following neuroleptanesthesia using fentanyl. A comparative study using a placebo].

Little is known about the effects of mixed opioid analgesics on gastrointestinal propulsion. In 20 patients, nalbuphine (0.1 mg/kg) was given after routine neuroleptanesthesia consisting of 70 micrograms/kg droperidol, 7 micrograms/kg fentanyl, and N2O/O2 (3:1) ventilation, to study its effect on gastrointestinal motility in the postoperative period. For comparison, another group of patients (n = 20) undergoing similar interventions received placebo (0.9% NaCl) at the end of the procedure. Gastrointestinal transit time was determined by measuring the exhaled H2 concentration following gastric lactulose administration. As lactulose is degraded only in the cecum, resulting in the release of hydrogen, the arrival of the polysaccharide at the terminal ileum could thus be determined. Compared to placebo, gastrointestinal transit was significantly longer in patients after nalbuphine (mean transit time 270 min vs 380 min). Pain estimation by visual analogue scale (VAS 0-10) suggested an antagonistic effect at the 10th and 20th min postoperatively, as pain scores in the nalbuphine group were higher when compared to placebo (3.5 vs 1.8 and 2.5 vs 1.4). There was a similar pain score in both groups (1.3 vs 1.4) 30 min after drug administration. However, there was significantly better pain relief after nalbuphine (0.7 vs 1.4 and 0.7 vs 1.1) in the late postoperative period (120th and 240th min). When given after potent opioids, it must be borne in mind that the antagonistic effect of nalbuphine is initially apparent. The agonistic potency of the compound will come into effect around the 30th min post-injection. Delayed gastrointestinal transit after nalbuphine is explained by agonist-like effects on peripheral opioid receptors in the gut.

Adult↗
PubMed1998

Absence of rectoanal inhibitory reflex in a child with multiple endocrine neoplasia type 2B.

BACKGROUND: Patients with multiple endocrine neoplasia (MEN) type 2B inherently present with gastrointestinal motility disorders as well as medullary thyroid carcinoma, adrenal pheochromocytoma, and Marfanoid habitus. METHODS: The authors examined gut motility function in a 7-year-old girl with MEN type 2B who had suffered from chronic constipation and recurrent acalculous cholecystitis since infancy. RESULTS: Results of total gastrointestinal barium meal and enema studies showed marked hypoperistalsis of the gut and entire colonic dilatation. Histopathologic study results of the gut wall from the stomach, duodenum, and rectum showed hyperplasia of the submucosal and intramuscular neural plexuses in all specimens. Anorectal manometry demonstrated disarrangement of the internal sphincter rhythmic wave and a complete absence of the rectoanal inhibitory reflex. CONCLUSION: These data suggest that gut motility disorders in MEN type 2B are caused by inadequately organized autonomic nervous system activity that originates from hyperplasia of the enteric nervous system.

Adrenal Gland Neoplasms↗
PubMed2003

Gastroduodenal motility.

PURPOSE OF REVIEW: The neuromuscular function of the stomach and duodenum provides the mechanical forces that drive digestion and are responsible for sensations of satiety and of dyspepsia. This article reviews (1) the neuroendocrine factors controlling upper gastrointestinal motility, (2) noninvasive techniques to evaluate gastroduodenal motility, and (3) the pathophysiology and treatment of gastroparesis. RECENT FINDINGS: Nutrients in the duodenum inhibit gastric emptying via a feedback pathway that involves release of cholecystokinin and serotonin (5-HT) from neuroendocrine cells; both act peripherally, cholecystokinin via cholecystokinin A receptors and serotonin via 5-HT3 receptors. The dorsal vagal complex plays a central role in the gastric inhibition mediated by tumor necrosis factor-alpha. The construction of maps that define intestinal movements in time and space has now been extended to the stomach. MRI compares favorably with the barostat in assessing gastric volume accommodation to meals and drugs and has the advantage of being noninvasive and showing contractions. Gastroparesis is increasingly recognized as a complication of end-stage liver disease; ascites plays no role in this, but portal hypertension stiffens the gastric walls and creates hypoxic conditions that may interfere with the neuromuscular functions of the stomach. Promising for the treatment of gastroparesis are clonidine, sildenafil, and intrapyloric botulinum toxin. Electrical stimulation triggers a vagally mediated relaxation of the stomach. SUMMARY: Drugs may be designed that specifically act on 5-HT3, cholecystokinin, or TNF-alpha receptors. Spatiotemporal maps should boost the diagnostic yield from dynamic imaging of motility using ultrasound, computed axial tomography scan, or MRI and the understanding of the mechanical forces driving digestion. Symptomatic benefit in gastroparesis may derive more from improved accommodation than gastric emptying.

Journal Article↗
PubMedDate not supplied

Postoperative gastric rupture in children with cerebral palsy.

Children with cerebral palsy (CP) develop difficulties with swallowing and bowel motility, although the underlying etiology of these disorders is unclear. The authors identified three children treated at their institution in the past 6 years who developed severe gastrointestinal dysfunction leading to gastric rupture after orthopaedic surgery; all three had a history that included CP (subtype spastic quadriparesis), low cognitive function, and gastrointestinal motility disorders. All three cases were fatal; in two patients the diagnosis was made at autopsy. No case of postoperative gastric rupture has been identified in children undergoing orthopaedic surgery without concomitant CP at the authors' institution. In this case series, they describe the preoperative and postoperative course of these three children. Since the only cure for gastric rupture is prompt surgical attention, orthopaedists should consider gastric rupture in the differential diagnosis of a postsurgical CP patient who becomes acutely unstable.

Adolescent↗