How Atropine Slows Down The Effects of Nerve Gas Poisoning?

By Urbanaveed
15 Min Read

Atropine is an immediate treatment for nerve gas poisoning. Atropine is available in the market in different forms, such as liquid injections, solid tablets, ointments, etc. To use which form of atropine depends upon the locality of a body part. Injections and tablets are more common in usage with injections being the most effective ones. Atropine is not used to treat nerve gas poisoning. It has many other seminal purposes in the body. Well, these purposes will also be explained in this blog.

Sticking to the crux of nerve gas exposure, it is a very deadly gas that directly affects the individual’s ability to breathe. Some prominent examples of nerve gas agents are sarin, tabun, VX, Cyclosarin, and Soman. They all share the same working action; repression of an enzyme. Although it sounds minimal, this enzyme (acetylcholinesterase) has very decisive roles in body physiology.

Acetylcholinesterase is an enzyme that permits the breakdown of acetylcholine. To understand acetylcholine is the neurotransmitter of the cholinergic system. Acetylcholine controls various influential mechanisms in the body. Being a neurotransmitter, it is released at the synaptic cleft by cholinergic neurons. Nerve gases affect the activity of acetylcholinesterase which in turn leads to the accumulation of acetylcholine at synaptic gaps.

How Acetylcholine Aggregation Leads to Mortality?

To understand the mechanism of atropine, one should have a basic understanding of the mortality of acetylcholine aggregation. Following is the sequential list of events that occur when someone accidentally inhales or is exposed to nerve gases.

How do Nerve gases cause the Inhibition of Acetylcholinesterase Enzyme?

To understand this mechanism, I forgot to mention one focal point. Nerve gases that show an active response to atropine, belong to the chemical category of organophosphates. Nerve gases derive this name as the phosphate group is attached to the organic part of the chemical. This phosphate group does not deserve ignorance. Because this is the phosphate group of organophosphates that is responsible for inhibiting the action of acetylcholinesterase. The phosphate group forms a covalent bond to the active site of acetylcholinesterase. This, in turn, alters the functional flare of acetylcholinesterase. Thus, acetylcholinesterase becomes useless and cannot perform its function of breaking acetylcholine into its substituents.

What Happens in Acetylcholine Aggregation?

Now, when acetylcholinesterase becomes non-functional. Acetylcholine begins to rise at neural junctions. The cholinergic system comprises the neurons and targets organs or glands that are responsive to acetylcholine. Acetylcholine is the primary component of the cholinergic system. As acetylcholine stimulates 3 types of receptors, these receptors are the integral units of the cholinergic system. These receptors are muscarinic-like receptors, nicotinic-like receptors, and receptors in the central nervous system (CNS). They have these attractive names due to their history of origins. Muscarinic-like receptors get their name from a mushroom (muscarine) and nicotinic-like receptors get their name from nicotine. As these receptors were initially found to be very responsive to these origins, maybe that became the reason for their special names. But first, let’s have a surface overview of Muscarinic-like receptors and nicotinic-like receptors. Because atropine medication is based upon its effects on these receptors.

Nerve Gas Poisoning and Muscarinic-like Receptors

Muscarinic-like receptors are spread almost all over the body’s responsive surfaces (cellular membranes that have receptors). They are present in a great number of nicotinic-like receptors whose presence is limited to certain body parts. The most prominent muscarinic-like receptors within the framework of nerve gas poisoning are smooth muscle cells of the vascular system, cardiac muscle cells, smooth muscle cells of the respiratory system, and receptors present in the central nervous system. Muscarinic-like receptors are also present in other body systems which control digestive motility, mucous secretions, bladder contractions, etc. These receptors are mostly aligned with the parasympathetic system. It means the physiological effects of these receptors facilitate the parasympathetic nervous system activation. So, from these insights, you can apprehend the function of muscarinic-like receptors and why their effects are mostly parasympathetic.

Similar Insights on Nicotinic-like Receptors

These receptors are not as much spread as muscarinic-like receptors. They are present only at neuromuscular junctions (NMJ), some sites in the autonomic nervous system. In nerve gas poisoning, neuromuscular junctions are the suffered victims. Acetylcholine aggregation at these junctions triggers muscle twitching, spasms, and irritability.

Excess Acetylcholine Receptors Stimulation impacts on cholinergic receptors in nerve gas poisoning or organophosphate poisoning
Symptoms associated with nerve gas poisoning due to overstimulation of cholinergic receptors.

Going Deep into the Effects of Nerve Gases on These Receptors

Nerve gases, when they block acetylcholinesterase activity, trigger the boost of acetylcholine at receptors. As muscarinic-like receptors are involved in bringing about the parasympathetic changes, acetylcholine aggregation at these receptors results in slow heart rate, difficulty breathing, digestive malaise, vasodilation, etc. Similarly, acetylcholine aggregation at skeletal muscle receptors has prominent effects on muscle hypercativeness. M2 receptors in the heart which are present at atrial walls, SA, and AV nodes, are sensitive to slow heart conduction or bradycardia. That is the reason, atropine proves effective in treating bradycardia. Well, this discussion will also be covered in this blog.

One of the highly fatal impacts of acetylcholine aggregation is on respiratory receptors. Respiratory hyperresponsiveness to acetylcholine is the highly contributing cause of death from nerve gas poisoning. Muscarinic-like receptors are accountable for causing bronchoconstriction (construction of bronchial airways)and mucus secretion in these airways. Bronchoconstriction and mucus secretion are the effects that are relevant to the parasympathetic system. For those who do not know about the parasympathetic nervous system, it is the combination of neurons and receptors that bring the body to resting or low active situations. The parasympathetic nervous system is very important when the body goes to hyperactive levels and then has to restore its original resting state.

So, bronchoconstriction and excessive mucus secretion become the cause of suffocation for the individual who has been exposed to nerve gases. In normal circumstances, acetylcholine breaks down at synaptic gaps but in this situation, its prolonged stimulation of muscarinic-like receptors in bronchial airways leads to these abnormal conditions. Individuals find it very difficult to breathe and body secretions, such as saliva, mucus, and gastric secretions begin to rise to abnormal levels.

Effects on Neuromuscular Junctions

Nicotinic-like receptors in muscles also become hyperactive and spur muscle fatigue due to prolonged contractions or muscles. Muscle fatigue or weakness occurs in relatively mild conditions, but when acetylcholine levels continue to rise, muscle twitching, especially in prominent facial muscles, happens. For those receptors who are present in the central nervous system, they also become active more than they need to be, giving rise to convulsions, spam, unconscious, and mental instability. It happens as acetylcholine activation is related to cognitive development and activeness of brain regions.

How Atropine Works in Nerve Gas Poisoning?

Atropine is the most recommended medication as a quick savior strategy for nerve gas poisoning. Its quickness lies in its ability to reduce the sensitivity of acetylcholine receptors. Atropine cannot bring down the levels of acetylcholine at receptors. Instead, it works as a competitive inhibitor. Competitive inhibitors simply repress the other molecule activity by being in excess. Atropine, when injected, starts to elevate at acetylcholine receptors. Being a competitive inhibitors, it shares the same structure as acetylcholine. So, acetylcholine receptors misunderstand the actual molecule and let atropine combine with them.

Atropine, when attached to acetylcholine receptors, does not provoke the physiological effects that acetylcholine causes. So, by this intelligent working action, atropine becomes successful in overcoming the excess of acetylcholine. But, atropine has one condition and that is its reversible nature. Atropine works as a reversible competitive inhibitors of acetylcholine. It cannot permanently inhibit acetylcholine receptors to take up acetylcholine.

How ATROPINE works in nerve gas poisoning and organophosphate poisoning?
In extended nerve gas exposure periods, continual supply of atropine is necessary as atropine effects are reversible and temporary.

It is only effective unless the atropine molecules are in more quantity than acetylcholine molecules. Once, atropine molecules get a lower number, acetylcholine again continues its binding to receptors. That’s why, atropine doses have to be given continually until the individual regains normal body physiology.

Atropine Uses to Treat Diseases Other Than Nerve Gas Poisoning

Atropine is similarly effective in treating bradycardia, bronchoconstriction, excessive gastric secretions, and frequent urine flow. Use of anticholinergics (such as atropine) can make the bladder to relax frequent urination. Its use suppresses acetylcholine attachment to the muscarinic-like receptors of these systems and lets these symptoms disappear for a while. Focusing on Bradycardia which is accustomed to acetylcholine stimulation of muscarinic-like receptors in the heart, it causes the slowness of heart contractions and conduction of signals from the SA node to the AV node.

More potassium efflux leads to arrhythmias and in turn, bradycardia. Acetylcholine receptors activate the release of potassium and inhibit the release of calcium to slow down the heart’s contractions. Atropine deactivates the acetylcholine effects on heart conductivity and brings the heart back to normal pace. Too much atropine can lead to tachycardia (fast heartbeats). So, the dosage of atropine is very sensitive in the case of bradycardia.

How Much Dosage of Atropine is Effective in Treating Nerve Gas Poisoning?

A dosage of atropine is only effective if the subject has mild or moderate nerve gas poisoning. In the cases of severe nerve gas poisoning, atropine alone would not bring effective changes.

Atropine Has No or Little Effect on Nicotinic-like Receptors

Atropine can act as a competitive inhibitor at muscarinic-like receptors and to a small extent, also for receptors in the central nervous system. But, it has almost non-influential effects on Nicotinic-like receptors. So, it cannot ease muscular paralysis. It has also little effect on respiratory restoration. If the subject is facing extreme difficulty in breathing, atropine alone cannot provide relief. In this condition, artificial respiration along with atropine dosages is much more effective than atropine alone. Artificial respiration can be given by the Holger-Neilson method.

How Much Dosage of Atropine and After What Intervals?

If it is not confirmed that the individual has nerve gas exposure, 2 mg of atropine is adequate at the initial stages. Atropine, in the form of injection, comes as atropine sulfate or tartrate. It can be administered through muscular, vascular, or oral routes, despite the vascular (injecting intravenously) route is much more effective and immediate in results than the other routes. The effects of atropine begin 1 minute after injecting intravenously, while it takes almost 8 minutes to show effects when injected through the muscular route.

The oral route is much slower. If the subject begins to show mild symptoms of atropinization after 2mg of atropine, then he has very little nerve gas exposure. Atropinization is the display of symptoms that occur due to the inhibition of muscarinic-like responses, such as dryness of mouth and esophagus, slowness in digestion, urinary constriction, slight tachycardia, and slight warmth.

The tolerance to show these symptoms rises with the increase of nerve gas exposure. The more the subject has nerve gas exposure, he needs more atropine to inhibit acetylcholine attachment to receptors. So, the dosage of atropine would increase after regular intervals.

If the atropinization symptoms do not appear after giving 2mg of atropine at regular intervals, the dosage of atropine can be raised to 4mg. If the mild symptoms of nerve gas poisoning are present, 2 mg. of atropine should be repeated after 20-30 30-minute intervals, but in the case of moderate symptoms, the dosage of atropine can be repeated and should be given at slightly fewer time intervals.

An authentic medical guide should be sought in giving dosage of atropine. In the case of prominent nerve gas poisoning, the atropine administration should be maintained for at least 24-48 hours.

This is Not a Professional Advice

The amount of dosage of atropine and after what intervals cannot be effective for all individuals. So, in the case of nerve gas poisoning, one must seek professional advice from a medical officer. This is just the general information regarding the minimum dosage of atropine and the general overview of time intervals. This information is shared to spread awareness about the effectiveness of atropine in the case of nerve gas poisoning.

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Student of BSc MLT at NUMS, and Content Writer in Health, Medicine, and Wellness. Finding soothe in writing and spreading knowledge.
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