Physicochemical properties and dosage regimens
Chemically, the drug is $\beta$-diethylaminoethyl ester of para-aminobenzoic acid. It is available as hydrochloride, which is highly soluble in water (1:1 ratio) and readily soluble in alcohol (1:8). When administered into tissues, it provides pronounced but short-lived analgesia.
The choice of solution concentration depends on the type of anesthesia performed:
- Infiltration anesthesia: 0.25–0.5% solutions are standardly used.
- A.V. Vishnevsky method (so-called tight creeping infiltration): the lowest concentrations are required — 0.125–0.25%.
- Nerve block anesthesia: 1–2% solutions are used.
- Spinal anesthesia: rarely used in modern practice; a high-concentration 5% solution is employed.
The drug is practically not used for surface anesthesia. This is due to the fact that it penetrates mucous membranes extremely poorly, and achieving an effect would require a concentration of about 10%.
Metabolic features and interactions
In the body, the drug undergoes relatively rapid hydrolysis. Plasma cholinesterase and various tissue esterases are involved in this process. The rationale for many of the drug's clinical effects and interactions is based precisely on the properties of the resulting breakdown products.
Upon molecule degradation, two key metabolites are formed:
- Para-aminobenzoic acid (PABA). It has a chemical similarity to sulfonamide drugs and acts as their competitive antagonist. If these drugs are used simultaneously, the local anesthetic will diminish the antimicrobial effect of sulfonamides.
- Diethylaminoethanol. This metabolite has a pronounced vasodilating effect. Due to local vasodilation, the absorption of the anesthetic itself into the blood is accelerated. This is an undesirable phenomenon, as it increases the risk of systemic toxicity and simultaneously reduces the duration of local analgesia.
To counteract the vasodilating effect of diethylaminoethanol, a vasoconstrictor (e.g., 0.1% epinephrine solution) is added to the solution. This slows down resorption, reduces the likelihood of toxic effects, and significantly prolongs local anesthesia.
Resorptive (systemic) action
When the drug is absorbed into the bloodstream, systemic effects develop, the primary direction of which is the depression of various body functions.
Effect on the nervous system and synaptic transmission The drug depresses visceral reflexes and suppresses polysynaptic spinal reflexes. It also exerts an anticholinergic effect: it reduces the release of the neurotransmitter acetylcholine from preganglionic fibers (autonomic ganglion blockade develops). In high doses, the drug is capable of reducing acetylcholine release from motor nerve endings, leading to impaired neuromuscular transmission.
Effect on smooth muscle and the cardiovascular system Upon entering the systemic circulation, the drug exerts a spasmolytic effect, reducing smooth muscle spasm of internal organs. Regarding the cardiovascular system, a hypotensive effect (decrease in blood pressure) and a short-term antiarrhythmic effect are observed. The latter is due to the drug decreasing myocardial automatism and excitability, as well as increasing its effective refractory period.
Briefly: answers to topical questions
What is the molecular mechanism of the local anesthetic action of procaine?
The molecular mechanism involves the reversible (non-covalent) blockade of voltage-gated sodium channels of the neuronal membrane. The drug dynamically binds to the channel protein structures, predominantly when they are in the activated (open) or inactivated state. This causes a blockade of sodium ion entry into the cell and prevents cell membrane depolarization, which ensures the temporary nature of anesthesia.
What are the contraindications to the use of procaine?
Contraindications to the use of procaine (Procainum) are:
- hypersensitivity to the drug or intolerance to local anesthetics;
- sulfonamide therapy;
- congenital pseudocholinesterase deficiency;
- myasthenia gravis;
- hypotension;
- administration into a focus of purulent inflammation.
The drug is used with caution in severe heart, liver, and kidney diseases.
How does the chemical structure of procaine differ from that of lidocaine?
The main difference lies in the type of chemical bond between the aromatic ring and the amino group.
| Characteristic | Procaine (Procainum) | Lidocaine |
|---|---|---|
| Chemical group | Esters | Substituted acid amides |
| Type of bond | Ester bond | Amide bond |
Due to these structural differences, the drugs are metabolized differently: procaine is rapidly hydrolyzed by plasma and tissue esterases, forming para-aminobenzoic acid, whereas lidocaine is biotransformed in the liver and does not form this metabolite.
What clinical symptoms develop in acute procaine overdose?
In acute overdose and intoxication with procaine (Procainum), symptoms develop that escalate as the drug concentration increases:
- Neurological disorders — dizziness, weakness, paresthesia, motor agitation, convulsions (including epileptiform ones).
- Autonomic disorders — skin pallor, sweating, nausea.
- Cardiovascular disorders — tachycardia, decreased blood pressure, collapse.
- Respiratory disorders — dyspnea, respiratory disorders up to apnea, pulmonary edema is possible.
The pathogenesis is based on impaired neuromuscular transmission and decreased acetylcholine release from motor nerve terminals.
To memorize the interaction: PABA — Suppresses Antibacterial Bacteriostatics (competes with sulfonamides, weakening their effect).
Class and exam questions
Why is procaine unsuitable for surface (terminal) anesthesia?
The drug penetrates intact mucous membranes very poorly. A high concentration (10%) is required to produce an effect, which makes this method impractical.
Why is epinephrine added to the procaine solution?
One of the drug's metabolites causes vasodilation, which accelerates its absorption into the bloodstream. Epinephrine vasoconstricts, slowing down resorption, prolonging anesthesia, and reducing the risk of toxicity.
How does procaine affect the efficacy of sulfonamides?
Hydrolysis of procaine yields PABA, which is a competitive antagonist of sulfonamides. When used together, the antimicrobial action of sulfonamides is weakened.
What else to study on this topic
- Classification of local anesthetics by chemical structure (esters and amides)
- Mechanism of action of sulfonamides and the role of PABA in folic acid synthesis
- Technique of tight creeping infiltration according to A.V. Vishnevsky
- Principles of neuromuscular blockade at high doses of local anesthetics
- The role of plasma cholinesterase and genetic aspects of ester anesthetic metabolism
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