Effect of Spinal Adrenergic and Cholinergic Antagonists for Antinociception of Intrathecal Gabapentin

2002 ◽  
Vol 42 (5) ◽  
pp. 677
Author(s):  
Myung Ha Yoon ◽  
Sung Su Chung ◽  
Hyeong Seok Kim
1980 ◽  
Vol 2 ◽  
pp. 257-267 ◽  
Author(s):  
Y.P. Tan ◽  
W. Stender ◽  
A.L. Harvey ◽  
B. Soria ◽  
F.J. Barrantes

2020 ◽  
Vol 6 (1) ◽  
pp. 7-14
Author(s):  
I. S. Drachev ◽  
V. I. Legeza ◽  
A. B. Seleznev

The paper describes the current state of development of seasickness as one of movement disease variants. The given type of pathology occurs when combining different types of ship’s motion (rolling and pitching). Circular, vertical and slow movements induce more pronounced and frequent signs of seasickness than linear, horizontal and quick ones. In the view of majority of researchers, the most likely is an intersensory conflict theory i.e. violation of coherent functioning of afferent body systems performing spatial orientation, statokinetic equilibrium and keeping balance. The leading role is played by the functional dysfunction of the vestibular analyzer. The classification of means of preventing and stopping of motion sickness is given, the mechanisms of their action, specific activity and side effects are described. It has been shown that currently the most effective drugs are M-cholinergic antagonists (scopolamine hydrobromide) and H1-histamine antagonists of the 1st generation (dimenhydrinate, diphenhydramine, cyclizine, meclizine, promethazine, etc.). Of the antipsychotics and blockers of D2 receptors, prochlorperazine and metoclopramide are recommended. It is also worth to use prokinetics (domperidone, cisapride, renzapride, etc.), tranquilizers (barbiturates, benzodiazepines), sleeping pills and local anesthetics. Particular attention is paid to combination drugs, consisting of antiemetic and psychostimulating drugs, designed to maintain working capacity under the influence of seasickness factors on the body. Non-pharmacological means of preventing seasickness and alleviating its symptoms are described. The main directions of improving the system of measures aimed at maintaining efficiency in the presence of symptoms of seasickness are determined. 


1980 ◽  
Vol 239 (3) ◽  
pp. G204-G209
Author(s):  
R. Ecknauer ◽  
W. J. Thompson ◽  
L. R. Johnson ◽  
G. C. Rosenfeld

The tritiated muscarinic cholinergic antagonist quinuclidinyl benzilate, [3H]QNB, was used as a direct probe for the detection and characterization of muscarinic cholinergic receptors associated with the particulate fraction of isolated and purified rat gastric muscosal parietal cells. Specific binding is saturable (Bmax = 55 fmol/mg protein, KD = 0.78 nM), shows a single population of binding sites, and has appropriate pharmacological specificity. Nanomolar concentrations of muscarinic cholinergic antagonists, such as atropine and scopolamine, inhibit [3H]QNB binding by 50%, whereas micromolar concentrations are needed for agonists, such as acetylcholine, oxotremorine, and carbamylcholine. Binding is also stereoselective as shown by the more than 1,000-fold difference in inhibitory potencies of the stereoisomers of benzetimide. Noncholinergic agents, including pentagastrin, histamine, and the H2-receptor antagonists cimetidine and metiamide, have little or no effect on [3H]QNB binding at concentrations of 100 microM. These data support the existence of specific parietal cell muscarinic cholinergic receptors with which the secretagogue acetylcholine may directly interact to initiate gastric acid secretion.


1987 ◽  
Vol 114 (4) ◽  
pp. 589-594 ◽  
Author(s):  
K. Hermansen ◽  
A. M. Kappelgaard

Abstract. The 40 aminoacids residue of pancreatic growth hormone-releasing hormone stimulates the secretion of insulin, glucagon, an somatostatin from the pancreas. To determine whether this stimulation of islet hormone secretion is mediated via adrenergic or cholinergic receptor sites, we studied the effects of 30 nmol/l of the growth hormone-releasing hormone on the release of insulin, glucagon, and somatostatin in the presence of either α-adrenergic (phentolamine), β-adrenergic (propranolol) or cholinergic (atropine) blocking agents. The responses to the growth hormonereleasing hormone were not significantly modified by adrenergic or cholinergic blockers. The findings rule out an interaction with adrenergic and cholinergic receptors on islet cells. It is at present unknown whether the growth hormone-releasing hormone stimulates islet hormone secretion via an interaction with specific growth hormone-releasing hormone receptors or vasoactive intestinal peptide receptors.


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