BACKGROUND: Antimuscarinic agents are used to block undesirable muscarinic effects of `anticholinesterase given to reverse the residual neuromuscular blockade produced by muscle relaxants. However, besides antimuscarinic effects, atropine was known to have some positive effects on the recovery from neuromuscular blockade by acting at the presynaptic muscarinic receptor of the neuromuscular junction. But there have been few reports about the neuromuscular effects of glycopyrrolate. So we observed the neuromuscular effects of atropine and glycopyrrolate, and compared two. METHODS: Mivacurium(0.064 mg/kg) was administered intravenously and the experimental groups were divided into 5 groups: the control group (no antimuscarinic agent administered), Al group (0.02 mg/kg atropine administered), A2 group (0.04 m atropine administered), Gl group (0.01 mg/kg glycopyrrolate administered) and G2 group (0.02 mg/kg glycopyrrolate administered). The left cammon peroneal nerve was stimulated by the 0.1 Hz single twitch and 100 Hz tetanic stimuli. We manitored the mechanical activity of the anterior tibialis muscle and observed recovery index, tetanic fade, and post-tetanic potentiation. RESULTS: There were no significant differences in recovery indices and post-tetanic potentiations among the 5 groups. Significant differences were found in tetanic fades between the experimental groups(A1, A2, Gl, G2) and the control group(P<0.05). However no significant differences in tetanic fades were found among the experimental groups. CONCLUSIONS: Atropine and glycopyrrolate hastened the recovery from mivacurium induced neuromuscular blockade. The neuromuscular recovery effects of glycopyrmlate were found to be similar to atropine at equipotent dose.
Atropine* ; Cholinergic Agents ; Glycopyrrolate* ; Muscarinic Antagonists ; Neuromuscular Agents ; Neuromuscular Blockade* ; Neuromuscular Junction ; Parasympathetic Nervous System ; Peroneal Nerve ; Receptors, Muscarinic ; Refractory Period, Electrophysiological

AIMTo investigate the roles of acetylcholine (ACh) receptors in the rapid effects of corticosterone (CORT) on the presympathetic neurons in the rostral ventrolateral medulla (RVLM) of rats, and study the non-genomic mechanism of glucocorticoid (GC) in the integration of sympathetic cardiovascular activity.

METHODSThe effects of microelectrophoresis of CORT on the discharge of the presympathetic neurons in the RVLM were observed by extracellular recording in urethane-anaesthetized rats. The responses of atropine (a blocker for M type of ACh receptor, ATR), d-tubocurarine (a blocker for N1 type of ACh receptor, d-TC) and hexamethonium (a blocker for N2 type of ACh receptor, C6) to the effects of CORT on the presympathetic neurons were investigated respectively.

RESULTSTotally 33 presympathetic neurons in the RVLM were recorded. Among them the firing rate of 25 (76%) presympathetic neurons was increased by microelectrophoresis of CORT. The effects of CORT were also positively correlated with the currents. In the other 8 presympathetic neurons, had was shown no effect after microelectrophoresis of CORT. In 10 presympathetic neurons, which discharge was increased by CORT, microelectrophoresis of ATR decreased the firing rate of these presympathetic neurons (P < 0.05), and did not fully block the excitatory effect induced by CORT. In both 7 and 6 presympathetic neurons, application of d-TC and C6 had no effect on these neurons respectively, and did not fully block the excitatory effect induced by CORT.

CONCLUSIONCORT had rapid excitatory effects on the presympathetic neurons in the RVLM, which effect might be independent on ACh receptors.

Animals ; Cholinergic Antagonists ; pharmacology ; Corticosterone ; pharmacology ; Electrophoresis, Microchip ; Male ; Medulla Oblongata ; drug effects ; physiology ; Neuromuscular Nondepolarizing Agents ; pharmacology ; Neurons ; drug effects ; physiology ; Nicotinic Antagonists ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Cholinergic ; physiology

Anticholinergic drugs block muscarinic receptors at the detrusor muscle of the bladder. It can cause urinary retention by contracting the bladder neck. Cases of hydronephrosis, bladder dilatation as a result of polydipsia while taking anticholinergic drugs have been reported, but very few cases of chronic renal failure can be found. We report a case of a polydipsic schizophrenic patient who, after taking anticholinergic drugs as antipsychotic drugs to treat his schizophrenia for a long time, presented with chronic renal failure due to functional obstructive uropathy in the absence of demonstrable anatomic causes of obstruction.
Antipsychotic Agents ; Cholinergic Antagonists ; Contracts ; Dilatation ; Humans ; Hydronephrosis ; Kidney Failure, Chronic ; Muscles ; Neck ; Polydipsia ; Receptors, Muscarinic ; Schizophrenia ; Urinary Bladder ; Urinary Retention

The anticholinesterase pyridostigmine is usually used as a reversal agent of non-depolarizing muscle relaxants in general anesthesia. Most adverse muscarinic effects of anticholinesterases are controlled by anticholinergics; however, there is still a potential for fatal cardiac complications. We report a case of cardiac arrest associated with coronary vasospasm that developed during emergence from general anesthesia in a 61-year-old male patient undergoing uvulopalatopharyngoplasty with preoperatively undiagnosed coronary vasospastic angina. Anticholinesterases should be administered with caution for neuromuscular blockade reversal, especially in patients with coronary vasospastic angina.
Anesthesia, General ; Cholinergic Agents ; Cholinergic Antagonists ; Cholinesterase Inhibitors ; Coronary Vasospasm ; Heart Arrest* ; Humans ; Male ; Middle Aged ; Muscle Relaxation* ; Neuromuscular Blockade ; Neuromuscular Nondepolarizing Agents ; Pyridostigmine Bromide*

BACKGROUND: The serotonin type 3 receptors are diffusely distributed in both the central and the peripheral nervous system. Physiological and pathophysiological processes thought to be mediated by this receptor include nausea and vomiting, peripheral nociception and central antinociception, conditioned aversion response to drugs, anxiety, and cognition. Because of the structural similarity between the nicotinic acetylcholine receptor and the 5HT3 receptor, we investigated the effects of clinically used neuromuscular blockers on the 5HT3 receptor function related with PONV. METHODS: A cDNA clone encoding the full length murine 5HT3a receptor was subcloned into an oocyte expression vector and 50 ng of cRNA transcribed in vitro injected per oocyte. After 24 72 h incubation, oocytes were placed into a recording chamber continuously perfused with frog Ringer's solution and electrophysiological recordings were obtained by the two electrode voltage clamp technique. Serotonin with or without the various drugs were bath applied by a computer controlled solenoid valve. Peak currents induced by the drug applications were measured and dose responses were obtained. RESULTS: The 5HT3 receptor expression in Xenopus oocyte was identified by the pharmacologic tools. Serotonin induced rapid inward currents, and thus was showed dose-dependent: KD = 2.5 micrometer, Hill coefficiency = 2.09. Inhibition by the neuromuscular blockers showed dose-dependence and their inhibitory potency on 5HT3 receptor (IC50) was in order of d-tubocurarine (0.046 micrometer) > vecuronium (16.32 micrometer) > gallamine (1,169 micrometer). CONCLUSIONS: There was a different inhibitory effect of nicotinic cholinergic antagonists, clinically used neuromuscular blockers, on the 5HT3 receptor and a judicious selection of them might contribute to reducing the incidence of PONV clinically.
Anxiety ; Baths ; Cholinergic Antagonists ; Clone Cells ; Cognition ; DNA, Complementary ; Electrodes ; Gallamine Triethiodide ; Incidence ; Nausea ; Neuromuscular Blockade* ; Neuromuscular Blocking Agents* ; Nociception ; Oocytes* ; Peripheral Nervous System ; Postoperative Nausea and Vomiting ; Receptors, Nicotinic ; RNA, Complementary ; Serotonin* ; Tubocurarine ; Vecuronium Bromide ; Vomiting ; Xenopus*

BACKGROUND: The serotonin type 3 receptors are diffusely distributed in both the central and the peripheral nervous system. Physiological and pathophysiological processes thought to be mediated by this receptor include nausea and vomiting, peripheral nociception and central antinociception, conditioned aversion response to drugs, anxiety, and cognition. Because of the structural similarity between the nicotinic acetylcholine receptor and the 5HT3 receptor, we investigated the effects of clinically used neuromuscular blockers on the 5HT3 receptor function related with PONV. METHODS: A cDNA clone encoding the full length murine 5HT3a receptor was subcloned into an oocyte expression vector and 50 ng of cRNA transcribed in vitro injected per oocyte. After 24 72 h incubation, oocytes were placed into a recording chamber continuously perfused with frog Ringer's solution and electrophysiological recordings were obtained by the two electrode voltage clamp technique. Serotonin with or without the various drugs were bath applied by a computer controlled solenoid valve. Peak currents induced by the drug applications were measured and dose responses were obtained. RESULTS: The 5HT3 receptor expression in Xenopus oocyte was identified by the pharmacologic tools. Serotonin induced rapid inward currents, and thus was showed dose-dependent: KD = 2.5 micrometer, Hill coefficiency = 2.09. Inhibition by the neuromuscular blockers showed dose-dependence and their inhibitory potency on 5HT3 receptor (IC50) was in order of d-tubocurarine (0.046 micrometer) > vecuronium (16.32 micrometer) > gallamine (1,169 micrometer). CONCLUSIONS: There was a different inhibitory effect of nicotinic cholinergic antagonists, clinically used neuromuscular blockers, on the 5HT3 receptor and a judicious selection of them might contribute to reducing the incidence of PONV clinically.
Anxiety ; Baths ; Cholinergic Antagonists ; Clone Cells ; Cognition ; DNA, Complementary ; Electrodes ; Gallamine Triethiodide ; Incidence ; Nausea ; Neuromuscular Blockade* ; Neuromuscular Blocking Agents* ; Nociception ; Oocytes* ; Peripheral Nervous System ; Postoperative Nausea and Vomiting ; Receptors, Nicotinic ; RNA, Complementary ; Serotonin* ; Tubocurarine ; Vecuronium Bromide ; Vomiting ; Xenopus*

Bethanechol, a cholinergic agonist, has been recommended for the management of peripheral anticholinergic side effects during the treatment of antipsychotic medications. But there have been few studies which have evaluated the drug interactions of antipsychotics and bethanechol, even the treatment effects of bethanechol on anticholinergic side effects. So the authors have evaluated whether psychopathology and plasma haloperidol and reduced haloperidol concentrations are significantly changed or not when bethanechol was administrated with maintained doses of haloperidol and other coadministrated drugs(such a benztropine). Also we have evaluated the abating effects of bethanechol on anticholinergic side effects during the treatment with haloperidol. Fifteen schizophrenics with higher than 5 of total score of anticholinergic side effects of 'Rating scale for side effect' were assigned to two groups, and bethanechol 30mg/day and 60mg/day were applied on each group for 4 weeks. The daily haloperidol dosages were fixed before 2 weeks of study. We assessed anticholinergic side effects by 'Rating scale for side effect' and psychopathology by BPRS, and plasma haloperidol and reduced haloperidol concentrations by HPLC at baseline, 2nd week and 4th week. The results were as followed. 1) There was no significant change of plasma haloperidol and reduced haloperidol concentration. 2) At baseline, the dosage of haloperidol showed significant correlation with the total score of anticholinergic side effect, but not at 2nd week and 4th week. 3) In 60mg/day group, dry mouth and the total score of anticholinergic side effects were significantly improved, but not in 30mg/day group. 4) There was no significant change of BPRS except withdrawal at 2nd week. These results suggest that coadministration of bethanechol influenced neither on psychopathology nor on plasma haloperidol and reduced haloperidol concentrations and that improved dry mouth and total score of anticholinergic side effects at 60mg/day.
Antipsychotic Agents ; Bethanechol* ; Cholinergic Agonists ; Chromatography, High Pressure Liquid ; Drug Interactions ; Haloperidol* ; Mouth ; Plasma* ; Psychopathology ; Schizophrenia

Prostatitis is a common syndrome that is confusing and frustrating for urologists. Chronic prostatitis/chronic pelvic pain syndrome(CP/CPPS) is the most common form of prostatitis. The etiology of CP/CPPS is unknown, but possibilities include infectious, autoimmune, neurological and psychiatric causes. Clinical, laboratory, and imaging evaluations for the patient presenting prostatitis can be categorized as basic or mandatory evaluations, further or recommended evaluations, and optional evaluations in selected patients. Evaluation can aid in diagnosis and follow-up of the patient's response to therapy. Treatment for CP/CPPS is empiric and limited by a lack of randomized, placebo-controlled clinical trials. Antimicrobials are commonly used to treat patients with prostatitis. Other commonly used drugs include alpha-adrenoceptor antagonists, anti-inflammatory drugs, tricyclic antidepressants, and anticholinergic agents. Also, minimally invasive procedures are considered in patients with CP/CPPS. Although much progress has been made in therapy, there is no distinct treatment for patients with CP/CPPS. It is possible to treat intractable patients with 'care' not 'cure'.
Antidepressive Agents, Tricyclic ; Cholinergic Antagonists ; Diagnosis ; Humans ; Pelvic Pain ; Prostatitis*

Urinary incontinence is an important lower urinary tract symptom that negatively affects the quality of life. Urgency incontinence (UI) is urine loss accompanied by urgency, which is the chief complaint of overactive bladder (OAB) syndrome. OAB is defined as urgency, with or without UI, usually with frequency and nocturia. In contrast, stress urinary incontinence (SUI) involves involuntary urine leakage caused by a sudden increase in abdominal pressure. Treatment for urinary incontinence depends on the type of incontinence, the severity, and the underlying causes. Treatment options fall into four broad categories: lifestyle intervention, bladder retraining and/or pelvic floor muscle training, pharmacotherapy, and surgery. Pharmacotherapy is often the first-line therapy for OAB/UI, either alone or as an adjunct to various nonpharmacological therapies. Effectiveness of anticholinergic drugs for OAB/UI has been assessed in various observational and randomized controlled trials. Despite their side effects, anticholinergics are the first-line agents for UI. Tricyclic antidepressants have complex pharmacological actions such as anticholinergic, alpha adrenergic, antihistaminic, and local anesthetic properties. Recently approved anticholinergics, solifenacin and darifenacin, are selective M3 antagonists that may have tolerable side effects. Transdermal oxybutynin may offer comparable efficacy with oral formulation but lower side effects. In the absence of an effective and well tolerated drug for SUI, pharmacological therapy for this condition has remained in the off-label prescription of some products, particularly estrogens and alpha-adrenergic agonists. Duloxetine is the drug of choice specifically aimed at SUI. This article outlines the current state and future development in pharmacological therapy for urinary incontinence.
Adrenergic alpha-Agonists ; Antidepressive Agents, Tricyclic ; Cholinergic Antagonists ; Drug Therapy ; Duloxetine Hydrochloride ; Estrogens ; Life Style ; Nocturia ; Pelvic Floor ; Prescriptions ; Quality of Life ; Solifenacin Succinate ; Urinary Bladder ; Urinary Bladder, Overactive ; Urinary Incontinence* ; Urinary Tract

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