Dimercaprol

Mechanism of action: molecular level

The drug Dimercaprol (Unithiolum) belongs to the group of specific antidotes and acts as an active donor of sulfhydryl (thiol, -SH) groups. Its mechanism of action is inextricably linked to the pathogenesis of cardiac glycoside intoxication.

The toxic effect of glycosides is due to their tight binding to the $Na^+,K^+$-ATPase enzyme of cardiomyocyte membranes. When administered into the body, Dimercaprol enters into a direct chemical reaction with the cardiac glycoside molecule. Due to the presence of free thiol groups, the antidote forms strong disulfide bridges with the toxin. As a result of this interaction, the glycoside molecule dissociates from the enzyme. The main outcome of this chemical reaction is the release of the $Na^+,K^+$-ATPase's own thiol groups, which are critically important for its normal function.

Pharmacological effects and indications

The key pharmacological effect of the drug is the complete restoration of the transport function of $Na^+,K^+$-ATPase. Reactivation of this enzyme allows cells to resume active ion exchange, leading to the gradual relief of poisoning symptoms.

According to the presented data, the main indication for prescribing the drug is specific antidote therapy for complications arising from cardiac glycoside treatment (glycoside intoxication).

The drug's role in combination therapy of complications

For the successful treatment of cardiac glycoside poisoning, Dimercaprol is used as part of combination therapy. It is important for students to understand how the antidote interacts with other treatment methods:

• Replenishment of electrolyte deficiency ($K^+$ and $Mg^{2+}$). After Dimercaprol releases $Na^+,K^+$-ATPase, the enzyme requires activators. Magnesium ions act as such activators. Therefore, Potassium chloride or combination agents (Panangin, Asparcam) are prescribed in parallel. Magnesium triggers the activity of ATPase, which is necessary for the active transport of potassium ions into cardiomyocytes.
• Combating calcium excess. To bind (chelate) $Ca^{2+}$ ions in the systemic circulation, edetate disodium (Trilon B) is administered intravenously.
• Correction of conduction disorders. If atrioventricular (AV) block develops, Atropine is the drug of choice. It blocks cardiac $M_2$-cholinergic receptors, eliminating the inhibitory effect of the vagus nerve (n. vagus) on the atrioventricular node, which leads to improved conduction.

Dosage forms and dosing rules

The drug is available in two forms:

1. Powder (substance).
2. 5% solution in ampoules of 5 ml volume.

Routes of administration: the solution can be administered subcutaneously (SC), intramuscularly (IM), and intravenously (IV). Dosage calculation is performed strictly individually, based on the patient's body weight. Standard regimen: 1 ml of 5% solution per every 10 kg of body weight.

Prescription Examples

Example prescription for a solution in ampoules for a 50 kg patient (5 ml of solution, i.e., 1 ampoule per administration, will be required):

Rp.: Sol. Unithioli 5% - 5 ml D.t.d. N. 10 in ampull. S. Administer intramuscularly 5 ml (based on 1 ml per 10 kg of body weight).

Example powder prescription:

Rp.: Unithioli 1,0 D.t.d. N. 10 S. According to the regimen, for preparing a solution.

Class and exam questions

What else to study on this topic

• Structure and functions of cardiomyocyte $Na^+,K^+$-ATPase.
• Mechanism of the toxic action of cardiac glycosides.
• The role of magnesium and potassium ions in maintaining the resting potential.
• Pharmacodynamics of Atropine in bradyarrhythmias and AV blocks.
• The principle of action of chelating agents using Trilon B as an example.

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Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.