How does nerve gas lead to respiratory paralysis?

SouravSeptember 23, 2024

Answer

Nerve gas, such as sarin or VX, leads to respiratory paralysis primarily through the inhibition of the enzyme acetylcholinesterase (AChE), which is crucial for the normal functioning of synaptic transmission at the neuromuscular junction. Here’s how this process unfolds:

1. Inhibition of Acetylcholinesterase:

• Role of AChE: Acetylcholinesterase is an enzyme that breaks down acetylcholine (ACh) in the synaptic cleft after it has been released from presynaptic neurons. This breakdown is essential for terminating the action of ACh and allowing the muscle to relax after contraction.
• Nerve Gas Action: Nerve agents inhibit AChE, leading to the accumulation of ACh in the synaptic cleft. This results in prolonged stimulation of the postsynaptic receptors.

2. Prolonged Activation of Nicotinic Receptors:

• Continuous Stimulation: With ACh not being broken down, nicotinic acetylcholine receptors on skeletal muscle cells remain continuously activated. This leads to sustained depolarization of the muscle fibers.
• Desensitization: Over time, the continuous presence of ACh causes the nicotinic receptors to become desensitized. When this happens, despite the ongoing presence of ACh, the receptors no longer respond effectively, leading to a failure in muscle contraction.

3. Impact on Respiratory Muscles:

• Respiratory Paralysis: The muscles responsible for breathing, including the diaphragm and intercostal muscles, become paralyzed due to the desensitization of nicotinic receptors. This paralysis prevents these muscles from contracting, leading to respiratory failure.
• Lack of Neural Control: The inability to contract these muscles means that the body cannot effectively inhale or exhale, resulting in a critical lack of oxygen and an inability to remove carbon dioxide from the bloodstream.

4. Systemic Effects:

• Autonomic Nervous System: Nerve agents can also affect the autonomic nervous system, leading to symptoms such as excessive salivation, lacrimation, urination, diarrhea, gastrointestinal distress, and increased bronchial secretions, further complicating respiratory function.