What are the detoxification characteristics and principles of atropine?

The detoxification mechanism of atropine is mainly as follows: blocking muscarinic receptors to rapidly reduce or eliminate M-like symptoms; Excite the central nervous system, improve respiratory function, raise body temperature, relieve cerebral vasospasm, etc., and help coma patients wake up; Prevents xanthine dehydrogenase from being converted into xanthine oxidase, reduces the generation of oxygen free radicals, and therefore has the effect of anti-lipid peroxidation and stabilizing the cell membrane; In large doses, catecholamines can be antagonized, so they can dilate arterioles, cause facial flushing, hand and foot warmth, etc., but it has no blocking effect on the nicotinic receptors of the motor endplate, so it cannot relieve muscle tremor. Early rapid atropine and continuous drug use are the basic principles of rational application of atropine, and mastering the dose and time of the first dose and repeated administration are the key to rational drug use.

M receptor blockers. Inhibits the secretion of glands, and the salivary glands and sweat glands are the most sensitive. The opposite eye dilates the pupil, increases intraocular pressure, and accommodates paralysis (leading to hyperopia).

Relaxes visceral smooth muscle, has a good effect on the detrusor muscles of the gastrointestinal tract, ureter and bladder, and has a weak effect on the bile duct and bronchi. For the cardiovascular system: Block the sinus node M receptor, relieve the inhibition of the vagus nerve on the heart, and increase the heart rate.

It can also fight the conduction block and arrhythmia of the atrial and atrioventricular junction caused by vagal hyperexcitation, and has little effect on the myocardium. Toxic concentrations can cause intraventricular block. The amount has no obvious effect on blood vessels and blood pressure, and the larger dose causes the dilation of blood vessels, and the large dose can relieve the spasm of small blood vessels when microcirculation is disordered, and dilate the peripheral blood vessels to improve microcirculation.

As the dose increases, the center changes from excitability to inhibition.

Dilate the pupils and lower the intraocular pressure! Standard Promise.

Mainly used for organophosphate poisoning antagonistic cholinesterase bar is not very sure.

Detoxification mechanism of atropine: blocking acetylcholine.

Atropine can be used for the rescue of organophosphate poisoning.

Detoxification mechanism: blocking M choline receptors (mechanism of organophosphate poisoning: organophosphates + acetylcholinesterase = phosphorylated cholinesterase decreases acetylcholinesterase activity, and the concentration of acetylcholine in the synaptic cleft increases, overexcites M and N receptors, and produces poisoning symptoms).

It is often used in combination with cholinesterase resurrection drugs such as pralidoxime chloride and pralidoxime iodolytica.

1) It is changed to maintenance dose after the disease is in remission or "atropineization".

2) "Atropineization" - dilated pupils, flushing of the face, decreased secretion of glands, dry mouth, mild restlessness, etc.

3) Poisoned patients with severe hypoxia are at risk of ventricular fibrillation when using atropine, and oxygen should be given at the same time.

4) For poisoned patients with increased body temperature, physical cooling should be carried out, and atropine should be used with caution.

5) When atropine is combined with cholinesterase resurrection, the dose of atropine should be appropriately reduced.

Gradual and repeated use of the drug in the early stages.

When rescuing pesticides (mostly organophosphorus pesticides) poisoning, the dose of atropine should be appropriately controlled according to the degree of poisoning. Due to the increased tolerance to atropine after organophosphate pesticide poisoning, severe poisoning must be given in sufficient amount early and injected intravenously for rapid effect. Later, according to the situation, the drug is administered regularly to make it atropine.

Indicators of atropinetization are: dilated pupils anteriorly; Dry mouth, **dryness; facial flushing; decreased or absent rales in the lungs; increased heart rate, etc.

The dose should be tapered as soon as the patient has an atropineation table and the dosing interval should be extended. On the other hand, care should be taken to avoid poisoning caused by atropine overdose. Atropine poisoning is manifested by dilated pupils, facial flushing, dryness, high fever, confusion, mania, hallucinations, delirium, convulsions, tachycardia and urinary retention.

In severe cases, coma and respiratory paralysis may occur, and the drug should be immediately discontinued for observation and rehydration to promote the excretion of poison. Pilocarpine should be used for detoxification if necessary.