This study was conducted to determine how much of a residua1 accommodation remained one hour after three instillations of atropine or homatropine in 384 eyes of younger Koreans. The amount of residual accommodation was measured by the blur point method, and the following results were obtained. 1) The average amount of the residual accommodation was 0.96 D under l% atropine and 1.42 D under 5% homatropine. 2) In comparing the two cycloplegic agents, 1% atropine was found to be more effective than 5% homatropine. 3) Residual accommodation under l% atropine and 5% homatropine showed gradually decrease in older patients. 4) No sex difference was found.
Accommodation, Ocular/*drug effects ; Adolescent ; Adult ; Atropa belladonna/*pharmacology ; Atropine/*pharmacology ; Child ; Female ; Human ; Korea ; Male ; *Plants, Medicinal ; *Plants, Toxic

BACKGROUNDThe neurogenic bladder dysfunction caused by spinal cord injury is difficult to treat clinically. The aim of this research was to establish an artificial bladder reflex arc in rats through abdominal reflex pathway above the level of spinal cord injury, reinnervate the neurogenic bladder and restore bladder micturition.

METHODSThe outcome was achieved by intradural microanastomosis of the right T13 ventral root to S2 ventral root with autogenous nerve grafting, leaving the right T13 dorsal root intact. Long-term function of the reflex arc was assessed from nerve electrophysiological data and intravesical pressure tests during 8 months postoperation. Horseradish peroxidase (HRP) tracing was performed to observe the effectiveness of the artificial reflex.

RESULTSSingle stimulus (3 mA, 0.3 ms pulses, 20 Hz, 5-second duration) on the right T13 dorsal root resulted in evoked action potentials, raised intravesical pressures and bladder smooth muscle, compound action potential recorded from the right vesical plexus before and after the spinal cord transaction injury between L5 and S4 segmental in 12 Sprague-Dawley rats. There were HRP labelled cells in T13 ventral horn on the experimental side and in the intermediolateral nucleus on both sides of the L6-S4 segments after HRP injection. There was no HRP labelled cell in T13 ventral horn on the control side.

CONCLUSIONUsing the surviving somatic reflex above the level of spinal cord injury to reconstruct the bladder autonomous reflex arc by intradural microanastomosis of ventral root with a segment of autologous nerve grafting is practical in rats and may have clinical applications for humans.

Anastomosis, Surgical ; Animals ; Atropine ; pharmacology ; Male ; Models, Theoretical ; Rats ; Rats, Sprague-Dawley ; Reflex, Abdominal ; drug effects ; physiology ; Trimethaphan ; pharmacology ; Urinary Bladder, Neurogenic ; physiopathology

Aged ; Atropine ; Electrocardiography ; Female ; Heart Rate ; drug effects ; Humans ; Male ; Muscarinic Antagonists ; pharmacology ; therapeutic use ; Preoperative Care ; methods ; Quinuclidines ; pharmacology ; therapeutic use

AIMTo study the effect of atropine, muscarinic cholinergic antagonist, on the central analgesic action of melatonin (MT) and to explore the mechanism of MT analgesia.

METHODSAs an indicator of visceral pain, the unit discharges of the neurons in the posterior group of thalamic nuclei (PO) were caused by stimulating the great splanchnic nerve (GSN) of the cat. The cranial stereotaxic and extracellular glass microelectrode record technique were used. The drugs were given through the intra-cranial-ventricle (icv).

RESULTS0.1% MT (10 micrograms.kg-1, icv) was shown to inhibit the unit discharge of the neurons in PO of the cat, whether the long latency or the short latency, which was evoked by stimulating GSN. The inhibition of 0.1% MT (10 micrograms.kg-1, icv) on the short latency discharge of neurons in PO was antagonized by 0.1% atropine (20 micrograms, icv). However, 0.1% atropine (20 micrograms, icv) did not show antagonistic effect on the inhibition of 0.1% morphine (5 micrograms, icv) at the same latency.

CONCLUSIONMT exhibited central analgesic action with mechanism different from morphine. It was suggested that the cholinergic system may be involved in analgesic process of MT.

Analgesics ; administration & dosage ; pharmacology ; Animals ; Atropine ; pharmacology ; Cats ; Electric Stimulation ; Evoked Potentials ; drug effects ; Female ; Injections, Intraventricular ; Male ; Melatonin ; administration & dosage ; pharmacology ; Morphine ; pharmacology ; Muscarinic Antagonists ; pharmacology ; Neurons ; physiology ; Splanchnic Nerves ; physiology ; Thalamic Nuclei ; drug effects ; physiology

We investigated the effect of alpha-adrenergic and cholinergic receptor agonists on Ca2+ current in adult rat trigeminal ganglion neurons using whole-cell patch clamp methods. The application of acetylcholine, carbachol, and oxotremorine (50 muM each) produced a rapid and reversible reduction of the Ca2+ current by 17+/-6%, 19+/-3% and 18+/-4%, respectively. Atropine, a muscarinic antagonist, blocked carbachol-induced Ca2+ current inhibition to 3 +/- 1%. Norepinephrine (50 muM) reduced Ca2+ current by 18 +/- 2%, while clonidine (50 muM), an alpha2-adrenergic receptor agonist, inhibited Ca2+ current by only 4 +/- 1%. Yohimbine, an alpha2-adrenergic receptor antagonist, did not block the inhibitory effect of norepinephrine on Ca2+ current, whereas prazosin, an alpha1-adrenergic receptor antagonist, attenuated the inhibitory effect of norepinephrine on Ca2+ current to 6 +/- 1%. This pharmacology contrasts with alpha2-adrenergic receptor modulation of Ca2+ channels in rat sympathetic neurons, which is sensitive to clonidine and blocked by yohimbine. Our data suggest that the modulation of voltage dependent Ca2+ channel by norepinephrine is mediated via an alpha1-adrenergic receptor. Pretreatment with pertussis toxin (250 ng/ml) for 16 h greatly reduced norepinephrine- and carbachol-induced Ca2+ current inhibition from 17 +/- 3% and 18 +/- 3% to 2 +/- 1% and 2 +/- 1%, respectively. These results demonstrate that norepinephrine, through an alpha1-adrenergic receptor, and carbachol, through a muscarinic receptor, inhibit Ca2+ currents in adult rat trigeminal ganglion neurons via pertussis toxin sensitive GTP-binding proteins.
Acetylcholine ; Adult ; Animals ; Atropine ; Carbachol ; Clonidine ; GTP-Binding Proteins ; Humans ; Neurons ; Norepinephrine ; Oxotremorine ; Pertussis Toxin ; Pharmacology ; Prazosin ; Rats ; Receptors, Muscarinic ; Trigeminal Ganglion ; Yohimbine

OBJECTIVE: To investigate the regulation of atropine to the expression and secretion of TGF-beta2 in retinal pigment epithelium (RPE) cells by observing the changes of those under different treatments of atropine and carbachol. METHODS: D407 cells were cultured conventionally and divided into 4 groups as follows: (1) An experimental group (Group A), cells were pretreated with 10(-4)-10(-8) mol/L atropine for 30 min, and then treated with 10(-5) mol/L carbachol; (2) a negative control group (Group B), cells were treated with 10(-4)-10(-8) mol/L atropine; (3) a positive control group (Group C), cells were treated with 10(-5) mol/L carbachol; (4) a blank control group (Group D). The concentration of TGF-beta2 in the supernate, and the level of TGF-beta2 mRNA and protein were measured by ELISA, RT-PCR, and Western blot after the 24-hour treatment. The data were analyzed by analysis of variance. RESULTS: The levels of TGF-beta2 mRNA and protein in the cytoplasm and the concentration of TGF-beta2 in the supernate in the experimental groups were lower than those of the positive control group. Atropine at 10-4 mol/L could completely inhibit the effect of carbachol at 10-5 mol/L. The effect of atropine was concentration-dependent (F=1,056.897,1,320.170, and 475.657; P<0.001). There was no change of TGF-beta2 level in the cytoplasm and supernate with the treatment of atropine alone (P>0.05). CONCLUSION Carbachol can promote the expression and secretion of TGF-beta2 in human RPE cells and atropine could reverse it effectively, suggesting that M receptor may be involved.
Adult ; Atropine ; pharmacology ; Carbachol ; pharmacology ; Cell Line ; Female ; Humans ; Male ; Muscarinic Antagonists ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Retinal Pigment Epithelium ; cytology ; metabolism ; Transforming Growth Factor beta2 ; genetics ; metabolism ; Young Adult

Alcohol beverages have been used since the dawm of history and the pharmacology of alcohol has been studied extensively and the question whether alcohol is a stimulant has long been debated. now there seems little couble that alcohol is a primarys and continuous depressant of the CNS, and the general pharmacologic action of alcohol on the body is one of depression. The effects of various concentrations and type of alcoholic beverages on the gastrointestinal motor and secretory functions are influenced by a number of factors such as the state by the digestive processes, the presence or absence or gastrointestinal diseases, the amount and type of food present, the degree of tolerance for alcohol, accompanying psychological factiors, and so forth. it is generally accepted that gastirc secretion is stimulated by ehanol, but effects of ethanol on the motility of the gastrointestinal tract has not been clarified yet. Hence the present study was undertaken to investigate the effects of ethanol on gastrointestinal motility. The rabbits of either sex, weighting about 2kg, were killed by air embolism after 72 hours deprivation of food except water. The stomach and duodenum were isolated and cut into two parts, i.e. antrum and duodenum. Each strip of antrum and duodenum, sized 0.5X2.0cm, was placed in temperature controlled uscle chamber(37 degrees C) Containing Tyrode's solution and its contractile movement was recorded on Grass Polygraph(Model 7) via force displacement transducer(FT.03). The results are summarized as follows: 1) The strips of gastric antrum and duodenum showed spontaneous regular movement through the experimental period. Administration of ethanol from 0.1 to 1.0% inhibited the amplitude and frequency of both strips with dose-dependent manner. Most strips of the duodenum and 6 strips of the antrum showed relaxations of tone by ethanol and 4 strips of the antrum showed increased tone. 2) Tonic contraction of antral strips by ethanol was abolished only by the combined pretreatment of atropine and chlorpheniramine, or atropine and cimetidine, not by the phentolamine, proproanolol, atropine, hexamethonium, chlorpheniramine or cimetidine alone. 3) Inhibition of antral and duodenal motility by ethanol was not abolished by anyy one of the receptor blocking agents such as adrenergic alpha and beta, buscarinic, or histaminergic H-1 and H-2 receptor blocking agents. By the above resutls, it may be concluded that ethanol inhibits the motility of the duodenum, but excites or inhibits the motility of the gastric antrum. It is likely that the inhibitory effect of ethanol is it derect action on the smooth muscle, and the excitatory effect is mediated by a mechanism related with histamine and acetylcholine.
Acetylcholine ; Alcoholic Beverages ; Atropine ; Beverages ; Chlorpheniramine ; Cimetidine ; Depression ; Duodenum* ; Embolism, Air ; Ethanol* ; Gastrointestinal Diseases ; Gastrointestinal Motility ; Gastrointestinal Tract ; Hexamethonium ; Histamine ; Muscle, Smooth ; Pharmacology ; Phentolamine ; Poaceae ; Pyloric Antrum ; Rabbits ; Relaxation ; Stomach

AIMTo study the vasodilation effect of atropine and its mechanism.

METHODSIsometric tension was recorded in isolated rat super mesenteric arteries precontracted by noradrenaline (NE) to study the vasodilation effect of atropine, and to investigate the role of endothelial cell and vascular smooth muscle cell on vasodilation.

RESULTSAtropine was shown to significantly dilate the endothelium-intact and endothelium-denuded arteries precontracted by NE. Nomega-Nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhabitor), indomethacin (cyclooxygenase inhibitor), propranolol (general beta adrenoceptor antagonist) and glibenclamide (ATP sensitive potassium channel inhibitor) showed no effect on vasodilation of atropine. Atropine did not affect the concentration-contraction curve of K+. However, atropine suppressed the contraction induced by NE and CaCl2, but not that by caffeine in the Ca+ -free Krebs solution.

CONCLUSIONAtropine showed significant vasodilation effect which may derive, in part, from endothelium. Besides, atropine could inhibit the receptor-mediated Ca2+ -influx and Ca2+ -release, which was inferred to the mechanism of atropine on vasodilation.

Animals ; Atropine ; pharmacology ; Calcium ; metabolism ; Calcium Chloride ; antagonists & inhibitors ; Cyclooxygenase Inhibitors ; pharmacology ; Endothelial Cells ; physiology ; Female ; In Vitro Techniques ; Indomethacin ; antagonists & inhibitors ; Male ; Mesenteric Artery, Superior ; drug effects ; NG-Nitroarginine Methyl Ester ; antagonists & inhibitors ; Nitric Oxide Synthase ; antagonists & inhibitors ; Norepinephrine ; antagonists & inhibitors ; Potassium Chloride ; antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Vasodilation ; drug effects ; Vasodilator Agents ; pharmacology

Spinal gabapentin has been known to show the antinociceptive effect. Although several assumptions have been suggested, mechanisms of action of gabapentin have not been clearly established. The present study was undertaken to examine the action mechanisms of gabapentin at the spinal level. Male SD rats were prepared for intrathecal catheterization. The effect of gabapentin was assessed in the formalin test. After pretreatment with many classes of drugs, changes of effect of gabapentin were examined. General behaviors were also observed. Intrathecal gabapentin produced a suppression of the phase 2 flinching, but not phase 1 in the formalin test. The antinociceptive action of intrathecal gabapentin was reversed by intrathecal NMDA, AMPA, D-serine, CGS 15943, atropine, and naloxone. No antagonism was seen following administration of bicuculline, saclofen, prazosin, yohimbine, mecamylamine, L-leucine, dihydroergocristine, or thapsigargin. Taken together, intrathecal gabapentin attenuated only the facilitated state. At the spinal level, NMDA receptor, AMPA receptor, nonstrychnine site of NMDA receptor, adenosine receptor, muscarinic receptor, and opioid receptor may be involved in the antinociception of gabapentin, but GABA receptor, L-amino acid transporter, adrenergic receptor, nicotinic receptor, serotonin receptor, or calcium may not be involved.
Acetic Acids/administration & dosage ; Acetic Acids/metabolism ; Acetic Acids/pharmacology* ; Adrenergic Antagonists/metabolism ; Adrenergic alpha-Antagonists/metabolism ; Analgesics/administration & dosage ; Analgesics/metabolism ; Analgesics/pharmacology* ; Animals ; Atropine/metabolism ; Dihydroergocristine/metabolism ; Enzyme Inhibitors/metabolism ; Excitatory Amino Acid Agonists/metabolism ; GABA Antagonists/metabolism ; Injections, Spinal ; Leucine/metabolism ; Male ; Mecamylamine/metabolism ; Muscarinic Antagonists/metabolism ; N-Methylaspartate/metabolism ; Naloxone/metabolism ; Narcotic Antagonists/metabolism ; Nicotinic Antagonists/metabolism ; Pain Measurement ; Quinazolines/metabolism ; Rats ; Rats, Sprague-Dawley ; Serine/metabolism ; Spinal Cord/drug effects* ; Thapsigargin/metabolism ; Triazoles/metabolism ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism