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Deadly brain attacks: Why do nerve agents cause such alarming symptoms?
Nerve agents, often called nerve gases, are a class of organic chemicals whose fundamental property is their ability to subvert the mechanism by which the nervous system transmits messages to organs. When nerve agents enter the body, they prevent the normal functioning of a key enzyme, acetylcholinesterase (AChE), which catalyzes the breakdown of acetylcholine. Due to the inability to break down acetylcholine, nerve signals are continuously transmitted and muscles continue to contract, eventually triggering a violent physiological reaction.
The first symptoms of nerve agents usually appear within 30 seconds of exposure, can cause suffocation or cardiac arrest, and can be fatal within minutes.
Initial symptoms of poisoning include runny nose, chest tightness and constricted pupils. As the poisoning worsens, the victim will face various physiological out-of-control conditions such as difficulty breathing, nausea, excessive salivation, and even a burning sensation in the eyes and lungs. The risk increases when muscles, especially those affecting the heart and breathing, are unable to receive signals to relax.
Survivors of poisoning almost invariably develop chronic neurological damage and associated psychopathological effects.
According to new research, the biological effects of these toxins are long-lasting and increase with continued exposure. In people with long-term exposure to nerve agents, levels of acetylcholinesterase in the serum and in red blood cells are significantly lower than normal, and the concentrations become lower the longer symptoms persist.
The mechanism of action of nerve agents involves that when normal motor nerves are stimulated, the nerves release acetylcholine, which transmits the signal to the muscles or organs, which is then broken down by the enzyme acetylcholinesterase to cause the muscles to relax. However, interference with the nerve agent halts this process, causing the muscles to continue to contract until muscle paralysis occurs throughout the body.
The current standard treatment for nerve agent poisoning combines anticholinergics with oxidants to manage symptoms and detoxify. Specifically, atropine acts as an anticholinergic drug and relieves symptoms by blocking the effects of excess acetylcholine.
Atropine is a standard anticholinergic drug whose dose is administered with the end criterion of clearing bronchial secretions.
To further mitigate the effects of nerve agents, pratoxine chloride (2-PAMCl) can reactivate acetylcholinesterase affected by the agent. Often in practice, military personnel carry these medications with them for self-administration in emergencies.
Finding effective preventive measures has become a top priority for the Department of Defense. For example, during the first Gulf War, the U.S. military used pyridostigmine bromide as a pre-treatment to increase the lethal dose of salin. But it's important to note that this drug is only effective if taken before exposure and may increase the risk of brain damage.
The history of the development of nerve agents can be traced back to 1936, when German scientists inadvertently created the first batch of nerve agents while trying to find new pesticides. Since then, nerve agents have gradually become a well-known and lethal weapon and are still used in military and terrorist activities in many countries.
When we face these horrific chemical weapons, how vigilant and prepared should we be to resist the threat of nerve agents?
