Atropine intravenous administration

Where musearinie symptoms are mild, supportive therapy may be suffieient. Severe eases will require intramuseular or intravenous administration of atropin. 

Another study of the effects of I on the cardiovascular systemic concluded that, in dogs anesthetized with sodium pentobarbital, the response of blood pressure to intravenous administration of I is a resultant of two separate effects a direct myocardial stimulation that was stopped with dichlorolsoproterenol and a stimulation of vascular smooth muscle that results in a slight increase in renal arterial pressure and a slight decrease in renal arterial flow. Neither atropine nor dichlorolsoproterenol affected these vascular effects. Injections of 1 into a jugular vein or a renal artery had no consistent effect on catecholamine concentrations in plasma taken from a femoral artery or a renal vein. In seven experiments in which I at 21-35 mg/kg was injected into a jugular vein, the mean blood pressure increased from 176/125 + 22/11... 

John H, Mikler J, Worek F, Thiermann H (2012) Application of an enantioselective LC-ESI MS/MS procedure to determine R- and S-hyoscyamine after intravenous administration of atropine to swine. 4 194-198... 

A report suggests that the intravenous administration of a cell-free extract of Anabaena flos-aquae (containing anatoxin-a) produced a transient vasodepressor response followed by a sustained rise in blood pressure in rats. Prolonged apnoea with attendant bronchoconstriction was observed, which remained unaltered by atropine. However, the statement by these authors that AN should be considered as a weapon of mass destruction, mainly due to its lethal anticholinesterase activity (Dube et al. 1996), raises the possibility of confusion with anatoxin-a(s) since AN is a nicotinic agonist and not a cholinesterase inhibitor. 

Gooding JM, Holcomb MC. Transient blindness following intravenous administration of atropine. Anesth Analg 1977 56(6) 872-3. 

Given that early responders may not know for certainty which nerve agent was responsible, patients suffering from nerve agent symptoms should receive pralidoxime immediately, in conjunction with atropine. The adult dose of pralidoxime (see Tables 3.3 and 3.4) is l-2g (15-25mg kg ) intramuscularly (18) or 1 g (15mg kg ) intravenously in lOOmL of saline over 15-30min. Intravenous administration, if possible, is preferable (3). After an hour, if paralysis persists, patients should receive a second dose (21). Severely iU adult patients may benefit from an intravenous 2g pralidoxime bolus followed by a maintenance infusion of 7.5mg kg h ... 

Intravenous administration of either one of the four pure compounds previously isolated from M. oleifera leaves (niazinin A, niazinin B, niazimicin and niaziminin A + B) in the concentration range of 1-10 mg/kg, produces hypotensive and bradycardiac effects in anaesthetized rats. Pretreatment of the animals with atropine (1 mg/kg) completely eliminates the hypotensive and bradycardiac effects of acetylchohne (ACh), whereas cardiovascular responses to the test compounds remains unaltered, ruling out the possible involvement of muscarinic receptor activation. In isolated guinea-pig atria all the compounds... 

Intravenous administration of norepinephrine in a patient already taking an effective dose of atropine will often... 

The LD50 value in mice from intravenous administration of tabun has been reported as 0.287 mg/kg (Tripathi and Dewey 1989). Gupta and coworkers (1987) investigated acute toxicity of tabun and its biochemical consequences in the brain of rats. An acute nonlethal dose of 200 pg/kg was injected subcutaneously. Within 0.5-1 hour, the toxicity was maximal it persisted for 6 hours, accompanied by a sharp decline in acetylcholinesterase activity. The prolonged inhibition of this enzyme in muscle and brain may be due to storage aud delayed release of tabun from nonenzymic sites. In addition, cyanide released from a tabun molecule could cause further delay in recovery from its toxic effects. Atropine and its combination with various compounds may offer protection against tabun (see Sections 39.2 and 39.3). 

Dogs were instrumented to examine the cardiac changes occurring for a month after intravenous administration of 2 LD50 of soman.113 Atropine and diazepam were administered shortly after soman exposure to control seizure activity. During the study period, there was an increased frequency of episodes of bradycardia with ventricular escape, second- and third-degree heart block, and independent ventricular activity (single premature beats,... 

Ventricular fibrillation, a potentially fatal arrhythmia, has been seen after administration of a ChE inhibitor and atropine. It can be precipitated by the intravenous administration of atropine to an animal that has been rendered hypoxic by administration of a ChE inhibitor.116117 Although this complication has not been reported in humans, atropine should not be given intravenously until the hypoxia has been at least partially corrected. 

Experimental studies117,159 have shown that when animals are poisoned with ChE inhibitors and then allowed to become cyanotic, rapid intravenous administration of atropine will cause ventricular fibrillation. Ventricular fibrillation after rapid intravenous administration of atropine has not been reported in humans. 

The direct injection of sarin into the pons and medulla of the rabbit produces tachypnoea, bradycardia, hypotension and respiratory arrest which are reversed by the intravenous administration of atropine [73]. Respiratory arrest also is produced when sarin is injected into the lateral reticular nuclei of the rabbit and bradycardia occurs following its introduction into the ventrolateral reticular formation, an effect which may be reversed by both atropine and vagotomy [73], This suggests these to be the target sites in the brain of the rabbit at which cholinesterase inhibition results in respiratory arrest and bradycardia. 

The LD50 of the compound atropine orally administered in rats is 500 mg/kg, and in mice is 75 mg/kg that after intravenous administration in rats is 73 mg/kg and in mice is 30 mg/kg. The LDgg of atropine in rats is 920 mg/kg after intramuscular administration and 280 mg/kg after intraperito-neal administration (Sax and Lewis 1992). 

Intravenous administration of 100, 300, or 1000 mg/kg of an alcohol extract of neem leaf to rats produced an initial bradycardia followed by cardiac arrhythmia. A significant and dose-related fall in blood pressure was observed and was immediate, sharp, and persistent. Pretreatment with either atropine or mepyramine did not alter the hypotensive activity of the neem leaf extract (Koley and Lai 1994). 

A comparison of the central nervous system levels and benefits achieved by intravenous administration of atropine and 2-PAM with those achieved by intramuscular injection performed 15-45 minutes earlier would provide important help in deciding upon the criteria for and amount of prehospital treatment to recommend. 

Introduction of a 0.01% solution of aceclidine into the conjunctival sac of rabbits reduced the pupil diameter on the average by 3 mm, the maximum myotic effect appearing in 20-30 minutes and having a duration of 1.5-2 hours. A 0.1% solution caused reduction of the pupil diameter by 5 mm and maximum myosis was produced by a 5-10% solution [122]. Administration of a 2% solution of aceclidine to rabbits 60 minutes after administration of a 2% solution of atropine sulphate removed mydriasis completely, the latter reappearing after 5 hours [127]. Aceclidine did not cause local anaesthesia [127]. After administration of a solution of aceclidine hydrochloride to rabbits the compound could be detected in the animal s blood serum [127]. Administered subcutaneously to rats at a dose of 25-50 mg/kg aceclidine caused intense salivation, lacrimation (chromodacryorrhea) and diarrhoea. Toxic doses produced tremors and convulsions. The acute LDgQ in rats was 45 mg/kg on intravenous administration, 225 mg/kg on subcutaneous administration [122] and 105 mg/kg when administered intraperitoneally [127]. The acute LDgo for white mice was 36 mg/kg, i.v. 112.5 mg/kg, s.c. and 165 mg/kg when administered per os [122]. In rabbits aceclidine at doses of 1 mg/kg i.v., 10 mg/kg s.c. and 25 mg/kg per os caused intense salivation, myosis and diarrhoea. 

A 60-year-old man with gastric carcinoma was given intravenous glycopyrrolate 10 pgfkg followed by ondansetron 4 mg as pre-medication for surgical operation. Within 2 minutes from ondansetron administration, the patient developed severe bradycardia (20 beats/min) associated with respiratory arrest and loss consciousness, which was resolved by intravenous administration of atropine 0.6 mg and ventilation with 100% oxygen. 

Well-known symptoms of sarin toxicity include miosis, hypersecretions, bradycardia, and fasciculations. However, the mechanism of organophosphate toxicity seems to involve conflicting actions. For example, mydriasis or miosis, and bradycardia or tachycardia may occur. Acute respiratory insufficiency is the most important cause of immediate death. Early symptoms include (i) tachypnea due to increased airway secretions and bronchospasm (a muscarinic effect), (ii) peripheral respiratory muscle paralysis (a nicotinic effect), and (iii) inhibition of respiratory centers (a CNS effect), all of which lead to severe respiratory deficiency. If left untreated at this stage, death will result. Cardiovascular symptoms may include hypertension or hypotension. Various arrhythmias can also occur, and caution is required when the QT interval is prolonged. In particular, if hypoxemia is present, fatal arrhythmias may occur with intravenous administration of atropine... 

Recommended doses of atropine are 2 mg in patients with mild symptoms that are primarily ocular, but without respiratory symptoms or seizures 4 mg in patients with moderate symptoms, including respiratory symptoms such as dyspnea and 6 mg in patients with severe symptoms, including seizures and respiratory arrest. The standard administration route should be intramuscular. As menhoned previously, intravenous administration of atropine in the treatment of severe symptoms such as hypoxemia can induce ventricular fibrillation thus, intramuscular administration is advised. Oxime agents such as 2-pralidoxime methiodide (2-PAM), or 2-formyl-l-methylpyridinium iodide oxime should also be given. The recommended dose for 2-PAM in... 

Specific treatment starts with the administration of atropine sulphate, a competitive antagonist of acetylcholine at muscarinic receptors. Sufficient atropine should be given to control hypersecretion and produce tachycardia and pupillary dilation. Very large doses of atropine are required atropine sulphate 2-A mg should be given intravenously every few minutes during the first hour, and then by continuous infusion. Patients may require up to 500 mg intravenously during the first day, and treatment may be needed for days. 

This drug is only approved for oral administration in some countries. It is effective for conversion of atrial flutter or fibrillation or ischaemia-induced ventricular arrhythmias. It has significant anticholinergic properties (10% of the potency of atropine) that can offset its direct depressant effects on sinus and AV nodes. It has a pronounced negative inotropic effect and should be administered with caution to patients with a history of congestive heart failure. For acute treatment of perioperative arrhythmias it is given intravenously 0.2 mg-kg-1 over 10-15 min, then 0.2 mg-kg-1 over the next 45 min and a maintenance infusion of 0.4 mg-kg-l-h-1. 

Treatment of test animals with anticholinesterase agents such as atropine and 2-PAM significantly reduced the acute lethality of diazinon in rats indicating that acute diazinon lethality is primarily attributable to the inhibition of acetylcholinesterase. Administration of 16 mg/kg atropine intramuscularly, with or without 30 mg/kg pyridine 2-aldoxime methochloride (2-PAM) given either orally or intravenously or both, to female albino rats 10 minutes before diazinon exposure increased the LD50 value (294 mg/kg) for diazinon for this species by a factor of 3.2 (with 2-PAM) or 1.7 (without 2-PAM) (Harris et al. 1969). 

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