Atropine as an Antidote

The role of atropine in toadstool poisoning

Poisoning by toxic mushrooms, such as toadstools, is accompanied by severe systemic intoxication. The pathogenesis is based on excessive receptor stimulation by muscarinic toxins. Treatment is built on two fundamental principles.

First, immediate decontamination is performed, which means removing unabsorbed toxin from the gastrointestinal tract. To achieve this, gastric lavage is performed, enterosorbents are administered to bind toxins, and saline laxatives are used to accelerate their elimination.

Second, specific antidote therapy is applied. The primary drug of choice here is atropine. Being a potent muscarinic antagonist, it binds to the receptors and reliably blocks them, thereby eliminating the dangerous muscarinic effects of the mushroom toxin.

Principles of competitive antagonism

To understand how antidotes work in pharmacology, it is necessary to examine the mechanism of competitive antagonism. This phenomenon is based on the direct competition of two different substances for binding to the same receptors in the body.

The outcome of this pharmacological contest is determined by two key factors:

1. Affinity is the natural affinity of a substance molecule for a specific receptor.
2. Concentration is the number of substance molecules in the synaptic cleft.

An important rule of competitive antagonism states that even if a toxic substance has a very high affinity, it can still be displaced from the receptor by another substance with a lower affinity. To achieve this, it is necessary to create a significantly higher concentration of the antagonist drug. Since the effect of a toxin or agonist can be completely neutralized and reversed by simply increasing the concentration of the competitor in the medium, this type of interaction is called surmountable antagonism.

Mechanism of action of physostigmine as an antidote

A classic example of the clinical application of competitive antagonism is the treatment of poisoning by atropine itself. Atropine is an M-cholinergic antagonist, and in its overdose, receptors become blocked.

To save the patient, a specific antidote is used—physostigmine. This is a drug from the anticholinesterase group. Its main feature is the ability to cross the blood-brain barrier, which makes it possible to eliminate toxic effects not only in the periphery but also in the central nervous system.

The mechanism of action of physostigmine unfolds in several stages:

• The drug blocks the enzyme cholinesterase, which normally degrades the neurotransmitter acetylcholine.
• Due to the cessation of degradation, the level of endogenous acetylcholine in the synapses begins to rise rapidly.
• Accumulated in huge quantities, acetylcholine enters into competitive struggle and successfully displaces atropine molecules from binding to M-cholinergic receptors, restoring normal nerve impulse transmission.

Another drug of this group, galantamine, has a similar central action.

Complex therapy for atropine poisoning

In addition to administering specific antidotes (pathogenetic therapy), the treatment of atropine intoxication requires large-scale detoxification measures and symptomatic support.

Detoxification measures (removal of the poison):

• Thorough gastric lavage using a potassium permanganate solution.
• Administration of adsorbents such as activated charcoal, as well as saline laxatives.
• Use of tannin or simply strong tea. These substances can chemically bind alkaloids (which include atropine) directly within the intestinal lumen.
• Active detoxification methods for blood purification: forced diuresis and hardware hemosorption.

Symptomatic therapy:

• To manage severe psychomotor agitation, the patient is administered tranquilizers (diazepam) or short-acting barbiturates.
• To maintain vital body functions in severe poisoning cases, the patient may be transferred to mechanical ventilation.

Ophthalmic use of physostigmine

In addition to toxicology, physostigmine is used in ophthalmology. Its main indication is angle-closure glaucoma; specifically, the drug is used for the emergency management of acute attacks of this condition.

The mechanism of therapeutic action is based on a pronounced miotic effect—the drug causes marked pupillary constriction. This leads to the mechanical opening of the anterior chamber angle and significantly facilitates the outflow of intraocular fluid.

In terms of clinical efficacy in reducing intraocular pressure, physostigmine significantly outperforms another popular drug, pilocarpine. However, it has a major drawback: the drug causes such a strong and abrupt contraction of the iris muscles that it often provokes pronounced pain syndrome in the eyes and the superciliary arch area.

Class and exam questions

What else to study on this topic

• Mechanism of muscarinic-like effects in mushroom poisoning
• Comparative characteristics of physostigmine and galantamine
• Indications for the use of short-acting barbiturates in toxicology
• Differences between overcome and insurmountable pharmacological antagonism
• Principles of hemosorption and forced diuresis

Other topics in the section «Drugs acting on cholinergic synapses»

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