Showing papers on "Atropine published in 2013"
TL;DR: VNS significantly reduced infarct size, improved ventricular function, decreased ventricular fibrillation episodes, and attenuated cardiac mitochondrial reactive oxygen species production, depolarization, and swelling, compared with the control group, suggesting the protective effects of VNS could be due to its protection of mitochondrial function during ischemia-reperfusion.
105 citations
TL;DR: In chicks, ocular growth inhibition is associated with choroidal thickening and growth stimulation with chOroidal thinning, suggesting a mechanistic link between the two responses, and the hypothesis that agonists would stimulate eye growth and thin the choroid was tested.
81 citations
TL;DR: Atropine 0.02% is the highest concentration that does not produce significant clinical symptoms from accommodation paresis or pupillary dilation, and would be an appropriate starting point in evaluating a low dosage of atropine to slow myopic progression.
Abstract: PurposeAtropine 1% has been used to slow the progression of myopia; however, it has not gained worldwide clinical acceptance because it results in clinically significant pupillary mydriasis and accommodative paralysis. Lower concentrations of atropine (0.5 to 0.01%) have been reported to be
71 citations
TL;DR: Sublingual atropine given as a single dose was not more effective than placebo in reducing the noise associated with death rattle.
40 citations
TL;DR: Atropine significantly reduced the prevalence of new arrhythmias during intubation particularly for children over 1 month of age, did not convert sinus tachy Cardia to ventricular tachycardia or fibrillation, and may contribute to the safety of intubations.
Abstract: OBJECTIVES Our objectives were to describe the prevalence of arrhythmia and conduction abnormalities before critical care intubation and to test the hypothesis that atropine had no effect on their prevalence during intubation. DESIGN Prospective, observational study. SETTING PICU and pediatric/neonatal intensive care transport. SUBJECTS All children of age less than 8 years intubated September 2007-2009. Subgroups of intubations with and without atropine were analyzed. INTERVENTION None. MEASUREMENT AND MAIN RESULTS A total of 414 intubations were performed in the study period of which 327 were available for analysis (79%). Five children (1.5%) had arrhythmias prior to intubation and were excluded from the atropine analysis. Atropine was used in 47% (152/322) of intubations and resulted in significant acceleration of heart rate without provoking ventricular arrhythmias. New arrhythmias during intubation were related to bradycardia and were less common with atropine use (odds ratio, 0.14 [95% CI, 0.06-0.35], p < 0.001). The most common new arrhythmia was junctional rhythm. Acute bundle branch block was observed during three intubations; one Mobitz type 2 rhythm and five ventricular escape rhythms occurred in the no-atropine group (n = 170). Only one ventricular escape rhythm occurred in the atropine group (n = 152) in a child with an abnormal heart. One child died during intubation who had not received atropine. CONCLUSIONS Atropine significantly reduced the prevalence of new arrhythmias during intubation particularly for children over 1 month of age, did not convert sinus tachycardia to ventricular tachycardia or fibrillation, and may contribute to the safety of intubation.
38 citations
TL;DR: The function of AA in improving GI motility is similar to that of SA, and this effect can be blocked by the presence of atropine, indicating that this effect is regulated by the vagus.
Abstract: Background Vagus nerve stimulation is capable of regulating autonomic nerve function. In Traditional Chinese Medicine, the effect of auricular acupuncture (AA) is mediated by the vagus. This study was designed to investigate the effect of AA on gastrointestinal (GI) motility and the relationship of this effect with the vagus nerve. Methods 50 rats were divided into five groups for observation of the effects of different types of acupuncture and influencing factors: control, AA, somatic acupuncture (SA), atropine and atropine+AA. The acupuncture points used for AA were ST (Stomach) and SI (Small intestine), while the acupuncture point used for SA was ST36. Electroacupuncture was performed for 15 min. A model of reduced GI motility was established using ethanol, and GI transit rate was used to measure GI motility. Heart rate variability (HRV) and the effect of atropine administration were investigated to study the relationship between AA and vagal activity. Results The GI transit rate increased in both the AA and SA groups compared with control, and no significant difference was found between their effects. In addition, after atropine administration, AA was found to be ineffective in influencing the GI transit rate. In the HRV analysis, no significant differences were found in the absolute low frequency normalised units, high frequency normalised units or the low frequency/high frequency component ratio in the AA or SA groups compared with control. After administration of atropine AA still had no effect on HRV. Conclusions The function of AA in improving GI motility is similar to that of SA, and this effect can be blocked by the presence of atropine, indicating that this effect is regulated by the vagus. However, HRV did not reflect the acupuncture-induced changes in vagal nerve function.
30 citations
TL;DR: The results suggest the involvement of CnF cholinergic system only on central blood pressure regulation that strongly mediated by muscarinic receptors.
27 citations
TL;DR: Analysis of the LY293558 pharmacokinetics after intramuscular administration showed that this compound readily crosses the blood–brain barrier and prevented neuronal loss in the amygdala and hippocampus, and reduced neurodegeneration in a number of brain regions studied 7 days after soman exposure.
Abstract: Control of brain seizures after exposure to nerve agents is imperative for the prevention of brain damage and death. Animal models of nerve agent exposure make use of pretreatments, or medication administered within 1 minute after exposure, in order to prevent rapid death from peripheral toxic effects and respiratory failure, which then allows the testing of anticonvulsant compounds. However, in a real-case scenario of an unexpected attack with nerve agents, pretreatment would not be possible, and medical assistance may not be available immediately. To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the GluK1 (GluR5)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid (LY293558) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman. We injected LY293558 intramuscularly, as this would be the most likely route of administration to humans. LY293558 (15 mg/kg), injected along with atropine and the oxime HI-6 at 20 minutes after soman exposure, stopped seizures and increased survival rate from 64% to 100%. LY293558 also prevented neuronal loss in the amygdala and hippocampus, and reduced neurodegeneration in a number of brain regions studied 7 days after soman exposure. Analysis of the LY293558 pharmacokinetics after intramuscular administration showed that this compound readily crosses the blood–brain barrier. There was good correspondence between the time course of seizure suppression by LY293558 and the brain levels of the compound.
24 citations
TL;DR: A significant decrease in the heart rate was noted, which is considered to be a critical effect of a low‐dose exposure to the atropine/scopolamine mixture, which may have serious implications if it occurred in people with pre‐existent cardiac conditions or those on medications that may cause bradycardia.
Abstract: To verify the assumptions in our previous risk assessment of an atropine/scopolamine mixture in buckwheat flour, we performed a randomized, double-blind, placebo-controlled cross-over study in 20 healthy, adult volunteers. The volunteers ingested a traditional Slovenian buckwheat meal, made of boiled buckwheat flour to which alkaloids were added. In addition to the placebo they ingested 0.12/0.10, 0.37/0.29, 1.22/0.95, 3.58/2.81 and 12.10/9.50 µg kg–1 body mass (BM) of the atropine/scopolamine mixture. The changes in body temperature, heart rate, salivary and sweat secretion, pupil size, near-point vision and subjective symptoms were recorded regularly for 4 h after the ingestion. Decreased salivary and sweat secretion, increased heart rate and pupil size and reduced near-point vision accompanied by characteristic subjective symptoms were observed at 12.10/9.50 µg kg–1 BM. At doses of 0.37/0.29 and 1.22/0.95 µg kg–1 BM, a significant decrease in the heart rate was noted, which we consider to be a critical effect of a low-dose exposure to the atropine/scopolamine mixture. Although this did not have any clinical relevance in our subjects, it may have serious implications if it occurred in people with pre-existent cardiac conditions or those on medications that may cause bradycardia. No significant changes in the observed end points were noted at 0.12/0.10 µg kg–1 BM. We estimate that the NOAEL (No Observed Adverse Effect Level) for the atropine/scopolamine mixture lies between the lower two administered doses. Applying the uncertainty factor of 10, we propose a new provisional Acute Reference Doses (ARfDs) of the mixture, i.e. 0.01 µg kg–1 BM for each alkaloid, and a further refinement using higher-tier approaches. Copyright © 2012 John Wiley & Sons, Ltd.
23 citations
TL;DR: This work adopted an in silico pharmacophore modeling strategy to develop features that are characteristics of known M1 subtype-selective compounds and used the model to identify several antagonists by screening an in-house (WRAIR-CIS) compound database.
16 citations
TL;DR: The antimuscarinic effect of MB327 was compared to that of established oximes and atropine in a rat jejunum smooth muscle model and showed a fully reversible smooth muscle relaxing effect at lower concentrations than all tested oximes.
TL;DR: The combination of a muscarinic agonist plus paclitaxel should be tested as a useful therapeutic tool in breast cancer treatment.
Abstract: Muscarinic acetylcholine receptors (mAChR) are expressed in cells without nervous origin. mAChR are up-regulated in tumor cells and their stimulation can modulate tumor growth. In this work we investigated the ability of mAChR activation to induce tumor cell death. We studied the action of a combination of low doses of the muscarinic agonist carbachol plus paclitaxel, a chemotherapeutic agent frequently used in breast cancer treatment, in terms of effectiveness. Long term treatment with carbachol exerted anti-proliferative actions on LM2 and LM3 murine mammary adenocarcinoma cells, similarly to paclitaxel. The combination of carbachol with paclitaxel at submaximal concentrations, added during 20 h decreased tumor cell proliferation in a more potent manner than each drug added separately. This effect was reverted by the muscarinic antagonist atropine, and was due to a potentiation of tumor cell apoptosis tested by TUNEL assay. This treatment did not affect the proliferation of the non tumorigenic mammary cell line NMuMG. In conclusion, the combination of a muscarinic agonist plus paclitaxel should be tested as a useful therapeutic tool in breast cancer treatment.
01 Nov 2013
TL;DR: It is found that culture media conditioned by pheochromocytoma cells stimulates proliferation of a human colon cancer cell line, an effect attenuated by atropine, a muscarinic receptor inhibitor.
Abstract: An elderly man with long-standing, nonresectable pheochromocytoma had rapid development of rectal adenocarcinoma despite close endoscopic surveillance. We determined that the patient's colorectal cancer overexpressed muscarinic receptor subtype 3, whereas his pheochromocytoma expressed choline acetyltransferase, an enzyme required to produce acetylcholine, which is a muscarinic receptor agonist. These findings suggested that acetylcholine release from the pheochromocytoma stimulated rapid growth of the rectal neoplasm. As proof of principle, we found that culture media conditioned by pheochromocytoma cells stimulates proliferation of a human colon cancer cell line, an effect attenuated by atropine, a muscarinic receptor inhibitor. Our observations provide both clinical and laboratory evidence that muscarinic receptor agonists promote the growth of colorectal neoplasia.
TL;DR: Treatment of AOP with CoQ10 + PAM + atropine in this animal model had a beneficial effect on both erythrocyte and heart tissue lipid peroxidation and AChE activity.
Abstract: The aim of this study was to examine the effects of ubiquinone (CoQ10) on heart tissue and erythrocytes in acute organophosphate poisoning (AOP). A total of 20 rabbits were divided into three groups: sham (n = 8), pralidoxime (PAM) + atropine (n = 6), and CoQ10 + PAM + atropine (n = 6). Blood samples were taken from each test subject to measure the values of acetylcholinesterase (AChE), nitric oxide (NO), and malondialdehyde (MDA) in the plasma and erythrocyte before administration of 50 mg/kg dichlorvos by orogastric tube. Blood samples were then taken at 1, 12, and 24 h post-dichlorvos to determine plasma and erythrocyte levels of AChE, NO, and MDA. Sham group received no treatment. PAM + atropine group received 0.05 mg/kg atropine with repeated doses and PAM: first a 30-mg/kg intravenous (IV) bolus, then a 15-mg/kg IV bolus every 4 h. CoQ10 + PAM + atropine group received same dose PAM and atropine and a 50-mg bolus of IV CoQ10. Thoracotomy was performed in all the animals 24 h after poisoning and then...
TL;DR: An inhibitory effect for the extract of A. millefolium was examined on muscarinic receptors of tracheal smooth muscle and a histamine (H1) receptor blockade was suggested for the Extract.
Abstract: Objective: To investigate one possible mechanism for the observed relaxant effect of A. millefolium (Achillea millefolium), in the present study the inhibitory effect of the extract of this plant on muscarinic receptors was examined. Materials and Methods: The effects of three concentrations of aqueous-ethanolic extract, 10 nM atropine, and saline on muscarinic receptors were tested in three conditions: In non incubated tracheal smooth muscle (group 1), tracheal chain incubated with propranolol and chlorpheniramine (group 2), and the one incubated with propranolol (group 3). Results: The EC 50 obtained in the presence of all three concentrations of the extract were significantly higher compared to saline in groups 2 and 3 (P Conclusion: These results showed an inhibitory effect for the extract of A. millefolium on muscarinic receptors of tracheal smooth muscle. A histamine (H 1 ) receptor blockade was also suggested for the extract.
TL;DR: Pralidoxime is a biochemical antidote that reactivates acetylcholinesterase by removing OP from it, and is effective in treating both muscarinic and nicotinic symptoms.
Abstract: Acute organophosphate (OP) poisoning produces cholinergic symptoms resulting from the inhibition of cholinesterase, and the overstimulation of muscarinic and nicotinic receptors in the synapses. The dominant clinical features of acute cholinergic toxicity include bradycardia, miosis, lacrimation, salivation, bronchorrhea, and bronchospasm. All symptomatic patients should receive therapy with oxygen, atropine, and pralidoxime. Atropine works as a physiologic antidote by competitively occupying muscarinic receptor sites, reducing the effects of excessive acetylcholine. Atropine should be immediately administered, and the dose can be titrated according to the severity of OP poisoning. A large dose may be necessary to overcome the excessive cholinergic state in case of severe poisoning. Pralidoxime is a biochemical antidote that reactivates acetylcholinesterase by removing OP from it. It is effective in treating both muscarinic and nicotinic symptoms. After some period of time, the acetylcholinesterase-OP compound undergoes a conformational change, known as aging, which renders the enzyme irreversibly resistant to reactivation by a pralidoxime. There has been a great deal of controversy over the effectiveness of pralidoxime in acute OP poisoning. However, it may be beneficial to administer pralidoxime for a sufficient period in case of severe poisoning with a large quantity of OP, which is common in Korea.
TL;DR: It is demonstrated that humoral catecholamine control of cardiovascular function was dominant over the immature parasympathetic nervous system in developing alligator embryos, and suggested that sympathetic and parASYmpathetic nerve terminals were present and developing in ovo but were not tonically active.
Abstract: We used arterial tyramine injections to study development of sympathetic actions on in vivo heart rate and blood pressure in embryonic, hatching and yearling female American alligators. Tyramine is a pharmacological tool for understanding comparative and developmental sympathetic regulation of cardiovascular function, and this indirect sympathomimetic agent causes endogenous neuronal catecholamine release, increasing blood pressure and heart rate. Arterial tyramine injection in hatchling and yearling alligators caused the typical vertebrate response — rise in heart rate and blood pressure. However, in embryonic alligators, tyramine caused a substantial and immediate bradycardia at both 70% and 90% of embryonic development. This embryonic bradycardia was accompanied by hypotension, followed by a sustained hypertension similar to the hatchling and juvenile responses. Pretreatment with atropine injection (cholinergic receptor blocker) eliminated the embryonic hypotensive bradycardia, and phentolamine pretreatment (α-adrenergic receptor blocker) eliminated the embryonic hypotensive and hypertensive responses but not the bradycardia. In addition, hexamethonium pretreatment (nicotinic receptor blocker) significantly blunted embryos' bradycardic tyramine response. However, pretreatment with 6-hydroxydopamine, a neurotoxin that destroys catecholaminergic terminals, did not eliminate the embryonic bradycardia. Tyramine likely stimulated a unique embryonic response — neurotransmitter release from preganglionic nerve terminals (blocked with hexamethonium) and an acetylcholine mediated bradycardia with a secondary norepinephrine-dependent sustained hypertension. In addition, tyramine appears to stimulate sympathetic nerve terminals directly, which contributed to the overall hypertension in the embryonic, hatchling and yearling animals. Data demonstrated that humoral catecholamine control of cardiovascular function was dominant over the immature parasympathetic nervous system in developing alligator embryos, and suggested that sympathetic and parasympathetic nerve terminals were present and developing in ovo but were not tonically active.
TL;DR: In this article, the efficacy of pralidoxime chloride and atropine for severe acute organophosphorus pesticide poisoning was investigated, including adverse effects, ICU stay, complications, and mortality.
Abstract: Objective This study aimed to clarify the efficacy of 2 therapies for patients with severe acute organophosphorus pesticide poisoning, including atropine adverse effects, the length of intensive care unit (ICU) stay, complications, and mortality. Methods A retrospective cohort study of 152 cases collected from May 2008 to November 2012 at 2 urban university hospitals was conducted. Patients admitted to the hospital for organophosphate poisoning were divided into 2 groups with different therapeutic regimens: group A was administered a repeated pulse intramuscular injection of pralidoxime chloride, and group B received the same initial dosage of atropine and pralidoxime chloride, but pralidoxime chloride intravenous therapy was administered for only 3 days, regardless of the length of atropine therapy. Subsequently, atropine adverse effects, length of ICU stay, complications, and mortality were statistically analyzed and compared between the 2 groups. Results The total dose of atropine was 57.40 ± 15.14 mg in group A and 308.26 ± 139.16 mg in group B; group A received less atropine than did group B ( P = .001). The length of ICU stay in group A was reduced ( P = .025), and group A had fewer atropine adverse effects ( P = .002). However, there was no significant difference in the mortality or complication rate between the 2 groups ( P > .05). Conclusion In patients with severe poisoning, group A used less atropine, had fewer atropine adverse effects, and had a shorter ICU stay. We suggest that therapy should be started as early as possible using a sufficient amount of pralidoxime chloride started intramuscularly in combination with atropine and that the drugs should not be prematurely discontinued.
TL;DR: The cholinergic antagonistic effects of a purifi ed mixture of tropane alkaloids extracted from Schizanthus hookeri competitively antagonized acetylcholine muscarinic receptors were evaluated in rat ileum.
Abstract: The relative lack of specificity of atropine as a competitive antagonist of muscarinic receptors is a frequent cause of undesirable parasympathetic side effects. Consequently, new tropane alkaloids with potentially greater selectivity are usually seen with real interest. The cholinergic antagonistic effects of a purified mixture of tropane alkaloids extracted from Schizanthus hookeri were evaluated in rat ileum. For this purpose, ileal segments were obtained from randomly selected male Sprague-Dawley rats, and the effect of 1 x 10(-4), 1 x 10(-3), and 1 x 10(-2) mg/mL of the purified mixture of alkaloids on the contractile response of the ileum induced with increasing doses of carbachol (5 x 10(-8) - 10(-4) M) was determined. The results were compared with those obtained in the presence of 3.46 x 10(-7), 3.46 x 10(-6), and 3.46 x 10(-5) mg/mL atropine as an agonist. Tropane alkaloids extracted from Schizanthus hookeri competitively antagonized acetylcholine muscarinic receptors.
TL;DR: Results suggest that in anaesthetized rats, BIMP induces powerful stimulation of sympathetic as well as parasympathetic nerves and thereby modulates heart rate and blood pressure, and may also indicate that an action independent of acetylcholinesterase inhibition contributes to the acute cardiovascular responses induced by BIMp.
TL;DR: The results suggest that EAAT3 knockout mice have a slower heart rate at rest, which may be caused by an increased parasympathetic tone possibly due to increased glutamate neurotransmission in the central nervous system.
Abstract: Parasympathetic tone is a dominant neural regulator for basal heart rate Glutamate transporters (EAAT) via their glutamate uptake functions regulate glutamate neurotransmission in the central nervous system We showed that EAAT type 3 (EAAT3) knockout mice had a slower heart rate than wild-type mice when they were anesthetized We design this study to determine whether non-anesthetized EAAT3 knockout mice have a slower heart rate and, if so, what may be the mechanism for this effect Young adult EAAT3 knockout mice had slower heart rates than those of their littermate wild-type mice no matter whether they were awake or anesthetized This difference was abolished by atropine, a parasympatholytic drug Carbamylcholine chloride, a parasympathomimetic drug, equally effectively reduced the heart rates of wild-type and EAAT3 knockout mice Positive immunostaining for EAAT3 was found in the area of nuclei deriving fibers for vagus nerve There was no positive staining for the EAATs in the sinoatrial node These results suggest that EAAT3 knockout mice have a slower heart rate at rest This effect may be caused by an increased parasympathetic tone possibly due to increased glutamate neurotransmission in the central nervous system These findings indicate that regulation of heart rate, a vital sign, is one of the EAAT biological functions
TL;DR: The results suggest that the positive inotropic action of ACh may be mediated by the activation of IP3 receptors through the stimulation of M3 receptors in the canine cardiac Purkinje fibers.
Abstract: Objective. The objective of this study was to investigate the inotropic mechanisms and the related muscarinic receptor subtype of acetylcholine (ACh) in canine cardiac Purkinje fibers. Materials and Methods. Isolated Purkinje fiber bundles were used for the measurement of contraction. The receptor subtype was determined using PCR and real-time PCR methods. Results. ACh evoked a biphasic response with a transient negative inotropic effect followed by a positive inotropic effect in a concentration-dependent manner. The biphasic inotropic actions of ACh were inhibited by the pretreatment with atropine. Caffeine inhibited the positive inotropic effect of ACh. ACh increased inositol-1,4,5-trisphosphate content in the Purkinje fibers, which was abolished by atropine. Muscarinic subtypes 2 (M2) and 3 (M3) mRNAs were detected in the canine Purkinje fibers albeit the amount of M3 mRNA was smaller than M2 mRNA. M1 mRNA was not detected. Conclusion. These results suggest that the positive inotropic action of ACh may be mediated by the activation of IP3 receptors through the stimulation of M3 receptors in the canine cardiac Purkinje fibers.
TL;DR: It is concluded that atropine eyedrops, administered sublingually for distressing upper respiratory secretions, may be an effective alternative to the injection of antimuscarinic drugs, or as an option when other antimuscarsinic formulations are not available.
Abstract: "Death rattle" is a term used to describe the noisy sound produced by dying patients caused by the oscillatory movements of secretions in the upper airways. Antimuscarinic drugs, including atropine, scopolamine (hyoscine hydrobromide), hyoscine butylbromide, and glycopyrronium, have been used to diminish the noisy sound by reducing airway secretions. We report on the effectiveness of sublingual atropine eyedrops in alleviating death rattle in a terminal cancer patient. We present a 58-year-old man with pancreatic cancer who was admitted to our hospital because of severe dyspnea, cough, and death rattle with excessive bronchial secretion as a result of multiple lung metastases. We administered 1% atropine eyedrops sublingually to obviate the need for subcutaneous infusions and to prevent somnolence. On the basis of our experience, we conclude that atropine eyedrops, administered sublingually for distressing upper respiratory secretions, may be an effective alternative to the injection of antimuscarinic drugs, or as an option when other antimuscarinic formulations are not available.
TL;DR: It is suggested that stimulation of the parasympathetic nervous system improves lymphocyte function during chronic stress by increasing mitogen-induced IL-2 production in rats under chronic stress.
Abstract: The purpose of this study was to clarify the effects of acetylcholine (Ach) on lymphocyte function in rats under chronic stress. The authors isolated peripheral lymphocytes from rats 5 weeks after stress treatment and then measured interleukin-2 (IL-2) production after stimulation with concanavalin A or phytohemagglutinin-L. Although mitogen-induced IL-2 production of the stress group was lower than that of the control group, the addition of Ach significantly increased mitogen-induced IL-2 production in both groups. This effect of Ach was inhibited by atropine in the control group only. The changes (increasing rates) in mitogen-induced IL-2 production from basal condition showed a negative correlation with serum corticosterone concentrations. The authors observed no correlation between the effects of Ach (changes in mitogen-induced IL-2 production with Ach compared to those without Ach) and serum corticosterone concentration. These findings suggest that stimulation of the parasympathetic nervous system im...
TL;DR: A 44-year-old female with no known history of any underlying diseases, developed a coronary spasm following ventricular tachycardia when 0.5 mg of atropine was injected intravenously to treat bradycardia during spinal anesthesia.
Abstract: Bradycardia may occur during spinal anesthesia with atropine commonly used as a treatment. A 44-year-old female with no known history of any underlying diseases, developed a coronary spasm following ventricular tachycardia when 0.5 mg of atropine was injected intravenously to treat bradycardia during spinal anesthesia. The imbalance caused by atropine in the sympathovagal activity may predispose the coronary artery to develop spasms with ventricular tachycardia. Therefore prudent use of atropine should be accompanied by close monitoring.
TL;DR: Activation of mAChRs by an exogenous agonist or elevation of endogenous ACh levels by an AChE inhibitor inhibits the non-cholinergic, atropine-resistant, component of reflexogenic bladder contractions in vivo.
11 Jul 2013
TL;DR: The analytical findings of atropine in the peripheral and heart blood from a case of suspected death reflect postmortem redistribution rather than cardiotoxicity, and have great implications for forensic toxicology.
Abstract: Atropine is an anticholinergic drug, used in treatment of spasm and pain. Postmortem blood atropine concentrations tend to be regionally
dependent. We reported in this work the analytical findings of atropine in the peripheral and heart blood from a case of suspected death. Atropine was determined in both peripheral and heart blood by liquid chromatography with tandem mass spectrometry. Towards the reference ranges, the concentration of atropine in the peripheral blood is therapeutic, and in the heart blood is lethal. The high concentration of atropine in the heart blood reflects postmortem redistribution rather than cardiotoxicity. The findings have great implications for forensic toxicology.
21 Nov 2013
TL;DR: The results suggest that TB is mediated by a complex sympathetic-parasympathetic interaction, which is immature during the vulnerable period and can potentially cause life-threatening cardiac events.
Abstract: Newborn infants and animals undergo dramatic development of the autonomic nervous system ; however, there remains a lack of normative information concerning the vulnerable period. This study investigated the maturation of the heart rate (HR) and the autonomic regulation of HR responses to restraint stress during the first 2 postnatal weeks in rats. Autonomic blockade with atropine, metoprolol, and dual atropine/metoprolol blockade (2 mg/kg) at postnatal day (P) 4 and P12 demonstrated predominantly sympathetic effects on baseline HR. From birth to P9, rats restrained by electrocardiography electrodes for 5 min displayed slow cardiodeceleration, which changed into transient bradycardia (TB) during P9-14. Interestingly, this TB was abolished by autonomic blockade on P12 ; stable tachycardia (18% increase) and unstable HR were observed under parasympathetic and sympathetic blockade, respectively. In addition, HR under dual blockade increased by 25% (p=0.009) after the animals were restrained but not under dual blockade with a 10-fold higher dose. These results suggest that TB is mediated by a complex sympathetic-parasympathetic interaction, which is immature during the vulnerable period and can potentially cause life-threatening cardiac events.
Journal Article•
TL;DR: Signs of severe hypermagnesemia due to an overdose of magnesium sulfate during an experimental study and its successful therapeutic outcome are described.
Abstract: A hypermagnesemic adult sheep during an experimental study showed gastraointestinal and respiratory changes
along with cardiovascular alterations included of obvious bradycardia and heart block. In order to save the animal
from fatal bradycardia, atropine sulfate was administrated instatntly at one dose 0.3 mg/kg. The animal was
survived and rhythm returned to sinus rhythm from marked bradycardia and sinus arrest after administration of
atropine. The present report describes signs of severe hypermagnesemia due to an overdose of magnesium sulfate
during an experimental study and its successful therapeutic outcome.
TL;DR: Acetylcholine relaxed phenylephrine-induced contractions of isolated rabbit prostate strips, and this relaxation may be mediated via both cholinergic and constitutive nitric oxide synthase with both the M2 and M3 receptors possibly playing key roles.
Abstract: Purpose: The location of acetylcholinesterase-containing nerve fibers suggests a role for acetylcholine in both contractility and secretion in the prostate gland. The colocalization of nitrergic nerves with cholinergic nerves, and the cotransmission of nitric oxide with acetylcholine in cholinergic nerves, has been demonstrated in the prostate glands of various species. Thus, we investigated the effects of acetylcholine on phenylephrine-induced contraction and the correlation between cholinergic transmission and nitric oxide synthase by using isolated prostate strips of rabbits. Materials and Methods: Isolated prostate strips were contracted with phenylephrine and then treated with cumulative concentrations of acetylcholine. Changes in acetylcholine-induced relaxation after preincubation with NG-nitroarginine methyl ester, 7-nitroindazole, and aminoguanidine were measured. The effects of selective muscarinic receptor antagonists were also evaluated. Results: In the longitudinal phenylephrine-contracted strip, the cumulative application of acetylcholine (10 -9 to 10 -4 M) elicited a concentration-dependent relaxation effect. Acetylcholine-induced relaxation was inhibited not only by nitric oxide synthase inhibitors (10 μM L-NAME or 10 μM 7-nitroindazole) but also by 10 μM atropine and some selective muscarinic receptor antagonists (10 -6