Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the effect of sympathetic denervation of the heart (removal of the stellate ganglion together with the sympathetic trunk up to the level of the 5th thoracic ganglion) on the ventricular fibrillation threshold (VFT) in dog. The acute experiments were performed under general anaesthesia with pentobarbital. Unilateral left sympathetic denervation raised the VFT to 144% of the initial value (14 measurements) and unilateral right sympathectomy to 214% (9 measurements). Immediately after bilateral denervation the VFT increased to 242% (23 observations). Atropine blockade of the vagus nerve (0.1 mg/kg b.w.) displayed no effect on the VFT increase. The observed increase in VFT corresponded with the finding that bilateral sympathetic denervation of the heart protected the dogs from spontaneous ventricular fibrillation after ligating the intraventricular branch of the left coronary artery. The authors compared their own results with those reported in the literature and discuss the possible clinical use of sympathetic denervation of the heart in the treatment of tachyarrhythmia.
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PMID:Antiarrhythmic effect of cardiac sympathectomy. 54 95

Clonidine infusion (10 microgram/kg, i.v.) elicited a 30% increase in repetitive extrasystole (RE) threshold in 6 chloralose-anesthetized dogs. A reduction in heart rate and arterial blood pressure accompanied the increased threshold. Intracisternal injection of clonidine (2 microgram/kg) in 6 dogs caused similar alterations in these parameters. Bilateral vagotomy, performed in 6 dogs prior to intravenous clonidine, prevented the increase in RE threshold but did not prevent the drug-induced bradycardia. Atropine (0.2 and 0.6 mg/kg), however, did not attenuate the effect of clonidine on RE threshold. Clonidine administration did not prevent the reduction in ventricular fibrillation threshold associated with a 10 min occlusion of the left anterior descending coronary artery or following reperfusion. We conclude that: (1) clonidine reduces ventricular vulnerability in the normal but not the ischemic heart, and (2) its protective effect is mediated by enhanced afferent vagal input to midbrain cardiovascular regulatory centers. This central nervous system action causes a reduction in sympathetic tone to the heart.
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PMID:Effects of clonidine on vulnerability to fibrillation in the normal and ischemic canine ventricle. 61 32

The objective of this study was to assess the changes in outcome of cardiac arrest due to ventricular fibrillation, asystole and electromechanical dissociation in relation to the changing guidelines for drug therapy set by the U.K. Resuscitation Council. It was a retrospective study of 667 resuscitation records for the years 1982, 1986, 1988, 1989, 1990 and 1991. It took place in a large district general hospital with a regional cardio-thoracic centre. We have audited the asystolic cardiac arrests (N = 271) which occurred outside the cardiac care unit (CCU). Adrenaline (intravenous 1 mg) is now the first line drug followed by atropine at an increased dose (2 mg intravenously); calcium is no longer recommended and sodium bicarbonate should be reserved for cases in which an acidosis has been documented. Atropine use has increased over the 9-year period. Bicarbonate use did not change from 1982 to 1986 but fell progressively to no use at all in 1991. Calcium use has declined since 1982. Adrenaline use has remained unchanged. Survival from asystolic arrests (hospital discharge) has remained unchanged at 0-5.5%. Asystole as a primary event in the CCU was uncommon (N = 17) and no patient was discharged. Over the same period, 60% of patients (N = 92) with a cardiac arrest on CCU due to ventricular fibrillation (VF) were discharged and 55% were alive after 6 months. For VF on the wards (N = 192), only 20% of patients were discharged from hospital. A similar proportion was successful for each year.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An audit of drug usage for in-hospital cardiopulmonary resuscitation. 133 43

Atropine can have a place during cardiopulmonary resuscitation (CPR) in the management of asystole, where parasympathetic influence might be excessive. However, the beneficial effects of atropine in electromechanical dissociation (EMD) have not been clearly demonstrated. The authors studied the effects of atropine in combination with epinephrine on an experimental model of EMD in the closed-chested dog. In 15 pentobarbital-anesthetized, mechanically ventilated dogs (mean weight 20 kg), EMD was induced by ventricular fibrillation followed by an external countershock, and was observed for 2 minutes before CPR was started. After 5 minutes of chest compression using a CPR thumper, either atropine 0.5 mg or D5W was administered, and the same injection was repeated every 5 minutes until recovery. Epinephrine 1 mg was administered in alternans. Each dog was submitted to two successive episodes of CPR, using either atropine or D5W, in a randomized order. Of a total of 28 CPRs, five were successful with chest compression alone. In the treatment groups, 10 of 11 were successful with atropine, but only eight of 12 with D5W (P < .01). The duration of CPR was also significantly shorter when atropine was used (9 minutes 56 seconds +/- 14 seconds versus 12 minutes 08 seconds +/- 43 seconds, P < .001). During the recovery period, atropine-treated animals had higher arterial pressure, heart rate, cardiac output and stroke volume. On this experimental model, the administration of high doses of atropine together with epinephrine enhances the recovery from EMD and results in a better cardiac function during recovery.
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PMID:Atropine administration in experimental electromechanical dissociation. 848 81

The purpose of this study was to evaluate the effects of the millimicrons opioid agonist D-Ala-2-Me-Phe-4-Gly-ol enkephalin (DAGO) on catecholamine-induced arrhythmias. Arrhythmias were produced, in the rat, by continuous infusion of epinephrine until the development of fatal arrhythmias that were usually ventricular fibrillation. Intracerebroventricular (ICV) administration of DAGO, 3 nmol, significantly (p less than 0.05) shifted to the right the relationship between epinephrine and both the onset of ventricular arrhythmias and the development of fatal arrhythmias. Naloxone, 1 mg/kg i.v., prevented these effects of DAGO. Atropine, 1 mg/kg i.v. or 20 micrograms/kg ICV, prevented the shift in these dose response relationships. Antagonism of DAGO's effects on arrhythmias could not be explained by an alteration of the blood pressure response to epinephrine. However, DAGO significantly increased blood pressure and decreased heart rate in separate experiments in animals that did not receive epinephrine and atropine prevent the heart rate and blood pressure effects of DAGO. These data show that 1) the millimicrons opioid receptor agonist DAGO suppresses epinephrine-induced arrhythmias, 2) the site of action can be within the CNS, 3) there is a role for the central parasympathetic nervous system to mediate the effect of DAGO and 4) endogenous opioids could modulate catecholamine-induced cardiac arrhythmias.
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PMID:Effect of D-Ala-2-Me-Phe-4-Gly-ol-5 enkephalin on epinephrine-induced arrhythmias in the rat and the interrelationship to the parasympathetic nervous system. 279 96

The hypothesis that elevation of intracellular guanosine 3':5' cyclic monophosphate (cyclic GMP) concentrations may increase electrical stability of the myocardium was examined by determination of ventricular fibrillation thresholds (VFT) on isolated perfused hearts of the rat. Hearts were paced to circumvent any complicating effects of bradycardia. Using this system, carbachol produced a concentration-related reduction in VFT. The reduction in VFT produced by carbachol was not significantly modified by a high concentration of atenolol (10(-5)M), indicating that the increased vulnerability to ventricular fibrillation was not an indirect consequence of catecholamine release from intramyocardial stores. Atropine (10(-6)M) blocked the carbachol-induced reduction in VFT. At the concentrations of carbachol used to reduce VFT, myocardial cyclic GMP concentrations were also elevated. The dibutyryl analogue of cyclic GMP (10(-4)M) mimicked the effect of carbachol in reducing VFT. Carbachol potentiated the adrenaline (3 X 10(-7)M)-induced reduction in VFT.
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PMID:Carbachol and dibutyryl cyclic GMP on the vulnerability to ventricular fibrillation in rat isolated hearts. 299 67

Tricyclic antidepressant drugs are known to cause often electrocardiographic abnormalities and to induce sometimes cardiac rhythm disturbances. We report a case of a patient on antidepressant therapy (Desipramine Hydrochloride, 50 mg/die, and Dothiepin Hydrochloride, 150 mg/die), without any underlaying heart disease, admitted to our Coronary Care Unit for recurrent syncopal episodes. An ECG on admission showed Sinus Tachycardia with Ectopic Ventricular Beats and recurrent runs of Torsade de Pointes, a distinctive form of Ventricular Tachycardia. Lignocaine i.v. was only transiently effective. Both Isoprenaline and Atropine Sulphate i.v. were uneffective. Ventricular Fibrillation occurred and cardioversion was achieved by a single DC shock. Amiodarone i.v. and electrical overdrive only temporarily suppressed ventricular arrhythmias. Magnesium Sulphate i.v. (bolus + infusion) induced a definitive suppression of Torsades de Pointes. One day later no more arrhythmias were present.
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PMID:[Torsade de pointes caused by tricyclic antidepressive agents. Description of a clinical case]. 355 44

Bradyarrhythmias, with or without hypotension, may be associated with acute myocardial infarction, especially inferior. The early use of atropine in the management of sinus bradycardia, with associated hypotension, spurred a continuing controversy that has found only partial solution in animal models. Experimentally there is increased sensory and autonomic motor activity with acute coronary occlusion. For example, in the cat, increased cholinergic activity was evidenced by the absence of bradycardia with atropinization and vagotomy, although these pretreatments accelerated the onset of significant ventricular arrhythmias. Atropine in experimentally infarcted dogs increased ischemia, while elevated heart rates reduced the threshold for ventricular fibrillation (VF) and vagal stimulation increased the threshold for VF, largely independent of heart rate. Specific clinical studies failed to support much of the animal data, although reports of tachyarrhythmias and VF resulting from the administration of atropine extended the controversy. The animal models, in the main, failed to mimic the clinical situation, for: 1) pentobarbital, with its propensity to alter some autonomic reflexes, dominated earlier work; 2) relatively large doses of atropine were employed; 3) the animals were presumed to be free of coronary and cardiac disease, factors known to influence autonomic reflexes; and 4) vagotomy and atropinization commonly preceded the acute occlusion.
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PMID:Atropine: animal models. 647 48

1. The potential use of catecholamines to increase the severity of dysrhythmias evoked by coronary artery ligation in the anaesthetized rat was investigated. Drugs were given intravenously prior to ligation. 2 Pressor doses of adrenaline (5 microgram/kg) noradrenaline (1 microgram/kg) phenylephrine (5-10 microgram/kg), and angiotensin (0.25 microgram/kg) conferred protection against the development of dysrhythmias. 3 Atropine (1 mg/kg) increased mortality from ventricular fibrilloflutter (VF) and abolished the protective effects of phenylephrine (10 micrograms/kg). 4 Administration of isoprenaline (10 microgram/kg) significantly increased the incidence of and the mortality from VF. 5 The order of antidysrhythmic drug potency of Org 6001 (1-10 mg/kg), disopyramide (2-10 mg/kg) and practolol (2-10 mg/kg) was similar in both the standard (without isoprenaline) and modified (with isoprenaline) models. 6 Use of the modified method for antidysrhythmic screening purpose allows demonstration of statistically meaningful results with the use of relatively few animals. 7 Comparison of the pattern of VF in the rat heart induced by various means suggests that the diagnosis of ventricular fibrillation can be made with more confidence in the modified method compared to the standard method.
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PMID:Development of a severe model of early coronary artery ligation-induced dysrhythmias in the anaesthetized rat. 727 92

The parotid glands and skin of the toad contain toxic substances. Ingestion of toad or toad cake may result in intoxication. Clinically, it may be predominantly manifested by a digitalis-like cardioactive effect. During the last six years, the National Poison Center of Taiwan has collected four cases of toad or toad cake intoxication: two cases were toad intoxication and two cases were toad cake intoxication. All four cases manifested with general weakness; three cases showed bradycardia, vomiting and diarrhea; two cases had numbness of the oral cavity; one case had excessive salivation; and two cases showed a consciousness change. In one case, an EKG showed bradycardia, and a first and second degree A-V block; this patient died of ventricular fibrillation. The prognosis in two cases was good. We lost contact with the last patient. The treatment principles in toad or toad cake intoxication is life support. If ingested, treatment is directed at prevention of absorption, including emesis, gastric lavage, activated charcoal and cathartics. Atropine, a pacemaker and other antiarrhythmic agents may be helpful in treating cardiovascular toxicity.
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PMID:[Toad or toad cake intoxication in Taiwan: report of four cases]. 790 65


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