These actions include vasodilation, drying of the mouth, an increase in the pulse rate, inhibition of contractions of the gastrointestinal tract, ureter, and bladder, and reduction of salivary, bronchial, gastric and sweat gland secretions. It does not prevent the release of acetylcholine but antagonizes the effect of acetylcholine on the effector cells. Atropine sulfate also acts peripherally as a competitive antagonist of the muscarinic actions of acetylcholine. This effect is manifested by mild central vagal excitation and moderate respiratory stimulation. Following the administration of usual clinical doses, atropine produces stimulation of the medulla and higher cerebral centers. It also has central nervous system activity, which may be stimulating or depressing depending upon the dose. The most important therapeutic action of atropine is the inhibition of smooth muscle and glands innervated by postganglionic cholinergic nerves. Evidence-based medicine for Chemical Defense - including efficacy and safety A. Chemical Defense therapeutic area(s) - including key possible usesĪtropine Sulfate is used for treatment of nerve agent poisoning and organophosphate pesticide poisoning. Name of Chemical Defense therapeutic agent/deviceĪtropine Sulfate 2. Pralidoxime chloride (2-PAM) is used as a cholinesterase reactivator that reactivates the enzyme to reduce accumulation of acetylcholine.ģ) Emetics, cathartics, and adsorbents to decrease further absorption.1. Atropine blocks receptors and is primarily used to reduce bronchoconstriction and raise the heart rate.Ģ) Cholinesterase reactivators. There are three categories of drugs used to treat organophosphate toxicity.ġ) Receptor–blocking agents. Blood/serum, liver, and urine can also be analyzed for residue of OPs or their metabolites. Frozen stomach and rumen contents should be analyzed for the pesticide. In addition to brain and skeletal muscles, OPs are known to adversely affect other organ systems, including the cardiovascular, respiratory, hepatic, reproductive and developmental, and immune systems.ĭiagnostic determination of organophosphate poisoning is often accomplished by confirming reduced acetylcholinesterase (AChE) activity in blood or brain. In acute poisoning, the primary clinical signs may be respiratory distress and collapse followed by death due to respiratory muscle paralysis. Severity and course of intoxication is influenced principally by the dosage and route of exposure. Onset of signs after exposure is usually within minutes to hours but may be delayed for >2 days in some cases. Some animals may have skeletal muscle tremors and subsequent weakness, loss in coordination and seizures. Usually the first to appear are hypersalivation, miosis (constricted pupils), frequent urination, diarrhea, vomiting, colic, and difficulty breathing due to increased bronchial secretions and bronchoconstriction. Poisoning from these pesticides results in cardinal clinical signs consistent with cholinergic stimulation. Organophosphates have a steep dose-response curve and should be handled and used cautiously. The effects may last weeks to months from a single exposure. They interfere with the action of a brain enzyme that breaks down the neurotransmitter acetylcholine. Pets and children are at risk of consuming the pesticide used in the household, and caution should be used when setting household baits to avoid accidental poisoning. Organophosphates are toxic to many species of birds and mammals including pets, farm animals, and wildlife species.Īlthough the targets are insects, non-target animals can ingest the products from open bait containers or indirectly become exposed by consuming poisoned insects or plant material. Organophosphates (OPs) and carbamates vary greatly in toxicity, residue levels, and excretion.
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