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atropine is optically inactive.

Small doses of atropine depress sweating and salivary and bronchial secretion. Atropine is particularly useful in relieving bronchoconstriction and salivation induced by anticholinesterases. Doses required to inhibit gastric secretion are invariably accompanied by dry mouth and ocular disturbances. At higher doses, the heart rate increases as the effects of vagal stimulation are blocked (Kentala et al.,1990). When given alone atropine has little effect on blood pressure, although it can block completely the hypotensive and vasodilatory effects of choline esters. Larger doses decrease the normal tone and amplitude of contractions of the bladder and ureter, thereby inhibiting micturition. Atropine inhibits both the tone and motility of the gut, reducing peristalsis.

Wood B, Haq EU (1971) An unusual case of atropine poisoning. Br J Clin Pract, 25: 469-470.

Other drugs with anticholinergic effects, such as tricyclic antidepressants, some antihistamines, phenothiazines, disopyramide and quinidine, will have additive peripheral and central nervous system anticholinergic activity if given with atropine (Dollery, 1991). Tertiary amine muscarinic receptor antagonists used as antispasmodics, such as dicyclomine, oxyphencyclimine, flavoxate and oxybutynin will also act similarly, as will quaternary ammonium muscarinic receptor antagonists, for example, ipratropium, methscopolamine and homatropine (Hardman, 1996).

THE ACTION MECHANISM OF RELAXATION EFFECT OF ATROPINE …

The muscarinic actions of parasympathomimetic drugs such as carbachol, bethanecol and pilocarpine are blocked by atropine (Hardman, 1996).

Atropine sulphate should be stored in single or multiple-dose containers, preferably glass, at a temperature of less than 40 °C (preferably between 15 to 30 ° C). It should be protected from light (McEvoy, 2002) and stored in airtight containers.(USP, 2002). Freezing should be avoided (McEvoy, 2002). The shelf-life is 24 months from the date of manufacturing if kept under the above conditions (personal communication, Abbott Laboratories, 1989).

Atropine is a muscarinic cholinergic blocking agent. It competitively blocks parasympathetic, postganglionic nerve endings from the action of acetylcholine and other muscarinic agonists. Atropinic drugs have little effect at nicotinic receptor sites. Large doses of atropine produce only partial block of autonomic ganglia and have almost no effect at the neuromuscular junction.

PDF Downloads : Oriental Journal of Chemistry

Harris WS, Goodman RM (1969) Hyper-reactivity to atropine in Down’s syndrome. New England Journal of Medicine, 279, 407-410.

In children, who received atropine 0.03mg/kg orally, peak plasma concentrations occurred at 90 minutes with only 10-20% occupancy of muscarine-2 subtype receptors. By contrast, after 0.02mg/kg intramuscular administration, peak was at 25 minutes with 60-70% receptor occupancy (Gervais et al, 1997). Following an oral dose of 0.03mg/kg atropine, a mean maximum serum concentration of 6.7nmol/L occurred at two hours in children, compared with 5.7 nmol/L at 30 minutes after intramuscular administration (Saarnivaara et al, 1985).

. Intramuscular absorption of atropine and atropine sulphate depends on the method of injection, the site of injection (Friedl et al, 1989) and the pharmaceutical form. Exercise may increase the rate of absorption (Kamimori et al, 1990). Atropine and atropine sulphate reach peak plasma levels when injected intramuscularly in about 30 minutes (Berghem et al, 1980, Saarnivaara et al, 1985, Gervais et al, 1997). In pregnant women at full term, however, mean peak plasma levels were reached at 1.59 hours, following a dose of 0.01mg/kg (Kanto et al, 1981). Absorption may be faster if atropine is injected into the deltoid muscle rather than the gluteal or vastus lateralis muscles (Ali-Melkkila et al, 1993). A study using time to peak heart rate to seek differences between routes of administration and pharmaceutical forms, found that intravenous administration was most rapid (5 5 minutes) compared to intramuscular administration of citrate buffered atropine in a modified syringe (26 + 13 minutes , citrate buffered atropine ( 40 + 15 minutes, or atropine sulphate (56 20minutes) (Martin et al, 1980).

Berman JM, Bertoldi IM (1985) Preparation of atropine sulphate ampoules for high dose therapy. Am J Hosp Pharm, 42: 1046.
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Journal of Nanoscience and Nanotechnology

Optimal drug doses and absorption parameters for administration by the endotracheal route are unknown (The American Heart Association, 2000) but medications should be administered at 2 to 2.5 times the recommended intravenous dose, and diluted before use in 10ml saline or distilled water in adults (Emergency Cardiac Care Committee, 1992). In children with normal cardiac status, Howard & Bingham (1990) found that there was no difference between effect on heart rate or speed of onset with either intravenous atropine sulphate 0.025mg/kg dilute in 2ml saline, given at the same time as 2ml saline endotracheally or twice the dose (ie 0.05mg/kg) of atropine given endotracheally at the same time as 2ml intravenously. After studying 50 patients using dose titration with endotracheal atropine, it was considered that if atropine must be given by the endotracheal route in an emergency, then 0.03mg/kg or more may be comparable to the effect of 0.01mg/kg given intravenously (Lee et al, 1989). Any route of vascular administration was considered preferable to the endotracheal route (The American Heart Association, 2000).

Hyzaar (hydrochlorothiazide/losartan potassium ..

After intravenous dosing, atropine distributes rapidly with only 5% remaining in the blood compartment after five minutes (Berghem et al., 1980). Initial distribution half-life is approximately one minute (Kanto & Klotz, 1988). Elimination kinetics can be fitted to a two-compartment model after therapeutic doses. The apparent volume of distribution (Vd) is 1-1.7 L/kg with a clearance of 5.9-6.8 ml/kg/minute and a half-life of 2.6-4.3 hours in the elimination phase (Kanto et al, 1981; Aaltonen et al., 1984; Virtanen et al., 1982).

TOXIC NEUROPATHIES - Neuromuscular Home Page

In microencephalic rats, compared to normal controls the magnitude of deficits in learning the Morris water maze increased as a function of atropine dose, suggesting that learning and memory may be related to changes in the number and/or function of muscarinic cholinergic receptors (Lee et al 1990). Behavioural alterations have been noted amongst the offspring of rats treated during pregnancy with atropine (Watanabe et al 1985).

Effect of external ACh and of atropine on - SpringerLink

After intravenous dosing, atropine elimination fits a two-compartment model with an intrinsic clearance of 5.9-6.8 ml/kg/min and a plasma half-life of 2.6-4.3 hours in the elimination phase (Kanto et al., 1981; Aaltonen et al., 1984; Virtanen et al., 1982).

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