Nature and Chemical Structure of Atropine
Atropine is an alkaloid naturally derived from plant sources. The primary natural sources of this compound include deadly nightshade (Atropa belladonna) and henbane (Hyoscyamus niger).
The ability of atropine to interfere with the nervous system depends directly on its chemical structure. The drug molecule bears a marked structural similarity to the endogenous neurotransmitter, acetylcholine. Specifically, the atropine structure contains an ester group and a nitrogen-containing fragment. This match in functional groups and their specific spatial arrangement allows the drug molecule to successfully compete with acetylcholine for binding sites on receptors.
Mechanism of Action and Effects of Atropine
By mechanism of action, atropine is a specific competitive antagonist of muscarinic ($M$) receptors. It physically blocks the binding of acetylcholine molecules to these receptors.
The primary pharmacological effect of this blockade is its action on the smooth muscle of internal organs. By preventing smooth muscle contraction, atropine causes marked relaxation, acting as a potent antispasmodic.
Clinical application of the drug is based on this effect:
- In ophthalmology, it is used for targeted relaxation of intraocular muscles, which is necessary for a thorough fundoscopic examination.
- In gastroenterology, the drug is essential for relieving acute spasms associated with gastrointestinal colic.
Adverse Effects of High Doses of Atropine
Using the drug in high doses carries the risk of serious adverse effects. Primarily, these are associated with the agent penetrating the central nervous system and affecting muscarinic receptors located there.
The main manifestations of high-dose toxicity include:
- Marked motor agitation;
- Psychological excitation;
- Hallucinations;
- Seizures.
Succinylcholine: A Curare-like Muscle Relaxant
Unlike atropine, succinylcholine (dithylinum) acts on a different group of receptors and serves as a competitive agonist of nicotinic ($N$) receptors. It belongs to the group of curare-like agents—a historical term for muscle relaxants derived from the initial discovery of these properties in curare poisons.
The primary site of action for succinylcholine is the neuromuscular junctions of skeletal muscles, which are rich in nicotinic receptors. The drug is also a structural analogue of acetylcholine and can bind directly to the receptors.
Mechanism of Persistent Depolarization
Although succinylcholine binds to receptors similarly to acetylcholine, its degradation in the synaptic cleft differs. The process of muscle relaxation occurs in several stages:
- The drug binds to nicotinic receptors.
- Unlike the endogenous neurotransmitter, succinylcholine is degraded very slowly by the enzyme acetylcholinesterase.
- Due to the prolonged presence of the agent in the synapse, ion channels remain open for an extended period, causing persistent membrane depolarization.
- As a result, nerve impulse propagation is completely disrupted, leading to profound muscle relaxation.
This specific effect is widely utilized in clinical practice during surgical procedures and complex endoscopic examinations where complete skeletal muscle relaxation is required.