piperidines and Paralysis

piperidines has been researched along with Paralysis* in 16 studies

Reviews

1 review(s) available for piperidines and Paralysis

ArticleYear
Prokinetic agents: a key in the future of gastroenterology.
    Gastroenterology clinics of North America, 1989, Volume: 18, Issue:2

    Prokinetic drugs enhance the motility of the luminal organs of the gastrointestinal tract. Few drugs developed in this decade are likely to have a greater impact on the treatment of disorders of the gastrointestinal tract. Bethanechol and metaclopramide have proven the potential utility of this class of drugs, whereas newer agents promise to have both a greater margin of safety and tolerability and a broader scope of utility. The efficacy of these agents is reviewed for the treatment of impaired motility from gastroesophageal reflux to severe chronic constipation.

    Topics: Biomechanical Phenomena; Cisapride; Domperidone; Forecasting; Gastroenterology; Gastroesophageal Reflux; Gastrointestinal Motility; Humans; Intestinal Diseases; Metoclopramide; Paralysis; Parasympathomimetics; Piperidines; Stomach Diseases

1989

Trials

1 trial(s) available for piperidines and Paralysis

ArticleYear
Effect of chronic administration of cisapride on gastric emptying of a solid meal and on dyspeptic symptoms in patients with idiopathic gastroparesis.
    Gut, 1987, Volume: 28, Issue:3

    In a double blind crossover comparison with placebo, the effects of cisapride (10 mg tid for two weeks), a non-antidopaminergic gastrointestinal prokinetic drug, on gastric emptying times and on symptoms were evaluated in 12 patients with chronic idiopathic dyspepsia and gastroparesis. Gastric emptying was studied by a radioisotopic gamma camera technique. The test meal was labelled in the solid component (99mTc-sulphur colloid infiltrated chicken liver). Nine symptoms (nausea, belching, regurgitations, vomiting, postprandial drowsiness, early satiety, epigastric pain or burning, heartburn) were graded weekly on a questionnaire. Cisapride was significantly more effective than placebo in shortening the t1/2 of gastric emptying (p2 = 0.04), but no significant difference was observed between the two treatments with regard to the improvement of total symptom score (p2 = 0.09). No side effects were reported during the study.

    Topics: Adult; Cisapride; Clinical Trials as Topic; Double-Blind Method; Dyspepsia; Female; Gastric Emptying; Humans; Male; Middle Aged; Paralysis; Piperidines; Stomach Diseases

1987

Other Studies

14 other study(ies) available for piperidines and Paralysis

ArticleYear
An agonist of the CXCR4 receptor accelerates the recovery from the peripheral neuroparalysis induced by Taipan snake envenomation.
    PLoS neglected tropical diseases, 2020, Volume: 14, Issue:9

    Envenomation by snakes is a major neglected human disease. Hospitalization and use of animal-derived antivenom are the primary therapeutic supports currently available. There is consensus that additional, not expensive, treatments that can be delivered even long after the snake bite are needed. We recently showed that the drug dubbed NUCC-390 shortens the time of recovery from the neuroparalysis caused by traumatic or toxic degeneration of peripheral motor neurons. These syndromes are characterized by the activation of a pro-regenerative molecular axis, consisting of the CXCR4 receptor expressed at the damaged site in neuronal axons and by the release of its ligand CXCL12α, produced by surrounding Schwann cells. This intercellular signaling axis promotes axonal growth and functional recovery from paralysis. NUCC-390 is an agonist of CXCR4 acting similarly to CXCL12α. Here, we have tested its efficacy in a murine model of neuroparalytic envenoming by a Papuan Taipan (Oxyuranus scutellatus) where a degeneration of the motor axon terminals caused by the presynaptic PLA2 toxin Taipoxin, contained in the venom, occurs. Using imaging of the neuromuscular junction and electrophysiological analysis, we found that NUCC-390 administration after injection of either the purified neuroparalytic Taipoxin or the whole Taipan venom, significantly accelerates the recovery from paralysis. These results indicate that NUCC-390, which is non-toxic in mice, should be considered for trials in humans to test its efficacy in accelerating the recovery from the peripheral neuroparalysis induced by Taipans. NUCC-390 should be tested as well in the envenomation by other snakes that cause neuroparalytic syndromes in humans. NUCC-390 could become an additional treatment, common to many snake envenomings, that can be delivered after the bite to reduce death by respiratory deficits and to shorten and improve functional recovery.

    Topics: Action Potentials; Animals; Elapid Venoms; Indazoles; Mice; Mice, Inbred C57BL; Motor Neurons; Neuromuscular Junction; Paralysis; Piperidines; Pyridines; Receptors, CXCR4

2020
Post-paralysis tyrosine kinase inhibition with masitinib abrogates neuroinflammation and slows disease progression in inherited amyotrophic lateral sclerosis.
    Journal of neuroinflammation, 2016, 07-11, Volume: 13, Issue:1

    In the SOD1(G93A) mutant rat model of amyotrophic lateral sclerosis (ALS), neuronal death and rapid paralysis progression are associated with the emergence of activated aberrant glial cells that proliferate in the degenerating spinal cord. Whether pharmacological downregulation of such aberrant glial cells will decrease motor neuron death and prolong survival is unknown. We hypothesized that proliferation of aberrant glial cells is dependent on kinase receptor activation, and therefore, the tyrosine kinase inhibitor masitinib (AB1010) could potentially control neuroinflammation in the rat model of ALS.. The cellular effects of pharmacological inhibition of tyrosine kinases with masitinib were analyzed in cell cultures of microglia isolated from aged symptomatic SOD1(G93A) rats. To determine whether masitinib prevented the appearance of aberrant glial cells or modified post-paralysis survival, the drug was orally administered at 30 mg/kg/day starting after paralysis onset.. We found that masitinib selectively inhibited the tyrosine kinase receptor colony-stimulating factor 1R (CSF-1R) at nanomolar concentrations. In microglia cultures from symptomatic SOD1(G93A) spinal cords, masitinib prevented CSF-induced proliferation, cell migration, and the expression of inflammatory mediators. Oral administration of masitinib to SOD1(G93A) rats starting after paralysis onset decreased the number of aberrant glial cells, microgliosis, and motor neuron pathology in the degenerating spinal cord, relative to vehicle-treated rats. Masitinib treatment initiated 7 days after paralysis onset prolonged post-paralysis survival by 40 %.. These data show that masitinib is capable of controlling microgliosis and the emergence/expansion of aberrant glial cells, thus providing a strong biological rationale for its use to control neuroinflammation in ALS. Remarkably, masitinib significantly prolonged survival when delivered after paralysis onset, an unprecedented effect in preclinical models of ALS, and therefore appears well-suited for treating ALS.

    Topics: Amyotrophic Lateral Sclerosis; Animals; Benzamides; Cell Death; Disease Models, Animal; Disease Progression; Encephalitis; Humans; Male; Motor Neurons; Mutation; Neuroglia; Paralysis; Piperidines; Protein Kinase Inhibitors; Pyridines; Rats; Rats, Transgenic; Spinal Cord; Superoxide Dismutase; Thiazoles

2016
Adenosine 2A receptor agonism: A single intrathecal administration attenuates motor paralysis in experimental autoimmune encephalopathy in rats.
    Brain, behavior, and immunity, 2015, Volume: 46

    A single intrathecal dose of adenosine 2A receptor (A2AR) agonist was previously reported to produce a multi-week reversal of allodynia in two different models of neuropathic pain in addition to downregulating glial activation markers in the spinal cord. We aimed to determine whether a single intrathecal administration of an A2AR agonist was able to attenuate motor symptoms induced by experimental autoimmune encephalopathy. Two A2AR agonists (CGS21680 and ATL313) significantly attenuated progression of motor symptoms following a single intrathecal administration at the onset of motor symptoms. OX-42, a marker of microglial activation, was significantly attenuated in the lumbar spinal cord following A2AR administration compared to vehicle. Therefore, A2AR agonists attenuate motor symptoms of EAE by acting on A2AR in the spinal cord.

    Topics: Adenosine; Adenosine A2 Receptor Agonists; Animals; Encephalomyelitis, Autoimmune, Experimental; Male; Microglia; Paralysis; Phenethylamines; Piperidines; Rats; Spinal Cord

2015
Suxamethonium and donepezil: a cause of prolonged paralysis.
    Anesthesiology, 2003, Volume: 98, Issue:2

    Topics: Aged; Anesthesia, General; Donepezil; Drug Interactions; Female; Fractures, Bone; Humans; Indans; Neuromuscular Depolarizing Agents; Nootropic Agents; Paralysis; Piperidines; Succinylcholine; Wrist Injuries

2003
[Sonographic studies during drug treatment of diabetic gastroparesis].
    Deutsche medizinische Wochenschrift (1946), 1988, Jun-16, Volume: 113, Issue:24

    Ultrasound examination of ten insulin-dependent diabetics with neuropathic gastroparesis demonstrated that gastric motility can be increased by intravenous injection of both cisapride and metoclopramide (Paspertin) (P less than 0.05 to less than 0.0005). During a one-hour period of observation stimulation lasted longer after cisapride than metoclopramide, but there were no qualitative differences between them. Compared with healthy subjects the frequency of antral contractions was increased after both drugs (P less than 0.05 and less than 0.025, respectively). Intensity and speed of contraction was less in patients than in the control subjects, but this effect was significant only for speed of contraction 20 min after injection of the drugs (P less than 0.05). The results indicate that ultrasonography makes it possible to monitor drug treatment of abnormal gastric emptying in diabetics by measurement of both frequency and degree of antral contraction.

    Topics: Adult; Cisapride; Diabetes Mellitus, Type 1; Diabetic Neuropathies; Female; Gastric Emptying; Gastrointestinal Motility; Humans; Male; Metoclopramide; Middle Aged; Muscle Contraction; Paralysis; Piperidines; Pyloric Antrum; Stomach Diseases; Ultrasonography

1988
Cisapride in postoperative gastroparesis.
    Lancet (London, England), 1987, Jan-03, Volume: 1, Issue:8523

    Topics: Acute Disease; Cisapride; Female; Humans; Middle Aged; Paralysis; Piperidines; Postoperative Complications; Stomach Diseases

1987
Biochemical basis of enhanced drug bioavailability by piperine: evidence that piperine is a potent inhibitor of drug metabolism.
    The Journal of pharmacology and experimental therapeutics, 1985, Volume: 232, Issue:1

    Piperine, a major active component of black and long peppers, has been reported to enhance drug bioavailability. The present studies were aimed at understanding the interaction of piperine with enzymatic drug biotransforming reactions in hepatic tissue in vitro and in vivo. Piperine inhibited arylhydrocarbon hydroxylation, ethylmorphine-N-demethylation, 7-ethoxycoumarin-O-deethylation and 3-hydroxy-benzo(a)pyrene glucuronidation in rat postmitochondrial supernatant in vitro in a dose-dependent manner. Piperine inhibition of these reactions in postmitochondrial supernatant from 3-methylcholanthrene- and phenobarbital-treated rats was similar to the controls. Inhibition by piperine of arylhydrocarbon hydroxylase (AHH) from 3-methylcholanthrene-treated rats was comparable to that observed with 7,8-benzoflavone. Piperine caused noncompetitive inhibition of hepatic microsomal AHH from the untreated and 3-methylcholanthrene-treated rats with a Ki of 30 microM which was close to the apparent Km of AHH observed in the controls. Similarly, the kinetics of inhibition of ethylmorphine-N-demethylase from control rat liver microsomes exhibited noncompetitive inhibition with an apparent Km of 0.8 mM and Ki of 35 microM. These studies demonstrated that piperine is a nonspecific inhibitor of drug metabolism which shows little discrimination between different cytochrome P-450 forms. Oral administration of piperine in rats strongly inhibited the hepatic AHH and UDP-glucuronyltransferase activities. The maximal inhibition of AHH observed within 1 hr restored to normal value in 6 hr. Pretreatment with piperine prolonged hexobarbital sleeping time and zoxazolamine paralysis time in mice at half the dose of SKF-525A. These results demonstrate that piperine is a potent inhibitor of drug metabolism.

    Topics: Alkaloids; Animals; Aryl Hydrocarbon Hydroxylases; Benzodioxoles; Biological Availability; Dose-Response Relationship, Drug; Ethylmorphine-N-Demethylase; Glucuronosyltransferase; Hexobarbital; Kinetics; Male; Mice; Microsomes, Liver; Paralysis; Pharmaceutical Preparations; Piperidines; Polyunsaturated Alkamides; Proadifen; Rats; Sleep; Zoxazolamine

1985
Diabetic gastroparesis and colonic dilatation treated with domperidone.
    Lancet (London, England), 1981, Feb-14, Volume: 1, Issue:8216

    Topics: Benzimidazoles; Domperidone; Gastrointestinal Hormones; Humans; Motilin; Paralysis; Piperidines; Stomach; Stomach Diseases

1981
Lisuride in parkinsonism.
    Annals of neurology, 1981, Volume: 9, Issue:1

    Lisuride is a soluble ergolene derivative with endocrine effects similar to but more potent than those of bromocriptine. In nine subjects with idiopathic, postencephalitic, or drug-induced parkinsonism, lisuride at a dosage of 0.05 to 0.15 mg intravenously caused an immediate improvement in tremor, rigidity, akinesia, and postural deformity, but also caused chorea and orofacial dyskinesia. Improvement lasted 2 to 3 hours. Lisuride had little or no effect in a single patient with progressively supranuclear palsy. Oral lisuride therapy, 0.8 to 4.8 mg daily, had similar effects but occasionally caused reduced awareness and hallucinations.

    Topics: Administration, Oral; Aged; Benzimidazoles; Chorea; Domperidone; Dose-Response Relationship, Drug; Drug Therapy, Combination; Dyskinesia, Drug-Induced; Ergolines; Female; Growth Hormone; Humans; Injections, Intravenous; Lisuride; Male; Middle Aged; Paralysis; Parkinson Disease; Parkinson Disease, Postencephalitic; Parkinson Disease, Secondary; Piperidines; Prolactin

1981
A study of the occurrence of anabaseine in Paranemertes and other nemertines.
    Toxicon : official journal of the International Society on Toxinology, 1971, Volume: 9, Issue:1

    Topics: Animals; Biological Assay; Colorimetry; Crustacea; Invertebrates; Paralysis; Piperidines; Pyridines; Species Specificity; Spectrophotometry; Tissue Extracts; Toxins, Biological; Venoms

1971
Sympatholytic treatment of "paralytic" ileus.
    Surgery, 1971, Volume: 70, Issue:3

    Topics: Antidepressive Agents; Butyrophenones; Carbamates; Catecholamines; Chlorpromazine; Diagnosis, Differential; Drug Synergism; Fluorine; Gastrointestinal Diseases; Gastrointestinal Motility; Humans; Ileum; Intestinal Diseases; Neostigmine; Paralysis; Piperidines; Pyridinium Compounds; Trifluperidol

1971
Pharmacological evidence for cholinergic processes in various central synapses.
    Proceedings of the Western Pharmacology Society, 1966, Volume: 9

    Topics: Animals; Cats; Electrophysiology; Heterocyclic Compounds; Muscle Spindles; Neuromuscular Junction; Paralysis; Parasympathomimetics; Physostigmine; Pilocarpine; Piperidines; Seizures; Strychnine; Synapses; Tachyphylaxis

1966
[CONTRASTS BETWEEN THE CENTRAL ACTIONS OF CONIINE AND STRYCHNINE].
    Archives internationales de pharmacodynamie et de therapie, 1964, Sep-01, Volume: 151

    Topics: Alkaloids; Animals; Birds; Cats; Cochlear Nerve; Cordotomy; Electric Stimulation; Electrocardiography; Electroencephalography; Gallamine Triethiodide; Paralysis; Pharmacology; Piperidines; Research; Seizures; Spinal Cord; Strychnine; Toxicology

1964
[On the treatment of spastic disorders with akineton].
    Therapie der Gegenwart, 1960, Volume: 99

    Topics: Biperiden; Humans; Muscle Spasticity; Paralysis; Piperidines

1960