Atropine mimic

Isoproterenol. Isoproterenol hydrochloride is an nonselective P-adrenoceptor agonist that is chemically related to NE. It mimics the effects of stimulation of the sympathetic innervation to the heart which are mediated by NE. It increases heart rate by increasing automaticity of the SA and AV nodes by increasing the rate of phase 4 diastoHc depolarization. It is used in the treatment of acute heart block and supraventricular bradyarrhythmias, although use of atropine is safer for bradyarrhythmias foUowing MI (86). 

Thus, the anticholinergic activity of the alkaloid hyoscyamine is almost entirely confined to the (—)-isomer, and the (+)-isomer is almost devoid of activity. The racemic ( )-form, atropine, has approximately half the activity of the laevorotatory enantiomer. An anticholinergic drug blocks the action of the neurotransmitter acetylcholine, and thus occupies the same binding site as acetylcholine. The major interaction with the receptor involves that part of the molecule that mimics acetylcholine, namely the appropriately positioned ester and amine groups. The chiral centre is adjacent to the ester, and also influences binding to the receptor. 

Acetylcholine, carbachol, and atropine. Naturally occurring acetylcholine and its synthetic agonists (e.g., carbachol) and antagonists (e.g., atropine) all share a methylated nitrogen atom which occupies receptor sites so as to mimic (carbachol) or block (atropine) the action of acetylcholine. 

Drugs chat mimic or oppose acetylcholine have a wide variety of uses. For instance, the muscarinic. agonist pilocarpine lowers intraocular pressure and antagonist atropine reverses vagal slowing of the heart. 

In the cestodes, H. dimimta, H. microstoma (17,34) and Grillotia erinaceus (35), ACh also relaxes longitudinal muscle strips or cut whole worm preparations. This suggests an inhibitory function. In G. erinaceus, carbachol mimics ACh, though nicotine is ineffective atropine is an ineffective antagonist of the ACh effect. 

Muscarinic agonists mimic the muscarinic effects of ACh and typically are longer-acting congeners of ACh or natural alkaloids that display httle selectivity for the various subtypes of muscarinic receptors. The muscarinic, or parasympathomimetic, actions of the drugs considered in this chapter are practically equivalent to the effects of postganglionic parasympathetic nerve impulses hsted in Table 6-1. AH of the actions of ACh and its congeners at muscarinic receptors can be blocked by atropine. 

Chlorpyrifos at 1.5-50 pg/ml (noncytotoxic les els) arrests DNA synthesis in undifferentiated cells, having less effect on RNA synthesis and liuLe on protein synthesis effect on DNA maximal at 1 hr these effects are not blocked by atropine or mecamylamine (moscarinic and nicotinic receptor antagonists, respectively) nicotinic (cholinergic) stimulation of undifferentiated cells does not mimic chlorpyrifos chlorpyrifos (50 pg/ml for I hr) inhibits residual DNA synthesis in differentiating cultures and robustly inhibits RN.A synthesis during early differentiation. 

The current model can simulate various endpoints for blood and tissues including free VX concentrations and B-esterase activity (AChE, BuChE and CaE). The model also has the capability to adjust cardiac output and tissue blood flows based on the level of brain AChE activity in order to mimic the physiological response to AChE inhibition. This adjustment assumes that cardiac output and tissue blood flows decrease over time by the same fraction as brain AChE activity. This adjustment is made when simulating data where the animals were not given atropine and were not artificially ventilated otherwise, the adjustment was not made. 

Symptoms of inappropriate or unintentional use (or accidental overdosage) of atropine autoinjectors used to treat nerve agent poisoning may mimic QNB exposure. However, marked confusion from atropine is not normally seen until a total of six or seven autoinjectors have been given. 

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