Lidocaine Hydrochloride Injection
Lidocaine Hydrochloride Injection

Lidocaine Hydrochloride Injection

Lidocaine Hydrochloride Injection is a local anesthetic of the amide group, available in injectable form. It has a wide range of applications for nerve blockade, including percutaneous infiltration, major nerve plexus block (e.g., brachial), epidural anesthesia, and intravenous regional analgesia.
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Products Specifications

 

Products Specification Vomume of vials Packing form
Lidocaine Hydrochloride Injection BP latest version 2/4/5ml transparent ampoule 10 or 100 amps/box

 

product-344-238
API mixing
product-370-239
Filling
product-367-244
Vial sterilization

 

Mechanism of Action: Lidocaine Hydrochloride Injection provides anesthesia through nerve blockade at various body sites and helps control dysrhythmias. It has a rapid onset of action (approximately one minute after intravenous injection and fifteen minutes after intramuscular injection) and spreads quickly through surrounding tissues. The duration of effect ranges from ten to twenty minutes (intravenous) and sixty to ninety minutes (intramuscular).

 

Absorption: Systemic absorption depends on injection site, dosage, and pharmacological profile. Maximum blood concentration occurs after intercostal nerve blockade, followed by lumbar epidural space, brachial plexus site, and subcutaneous tissue. The total injected dose determines absorption rate and peak anesthetic blood levels. Lipid solubility and vasodilator activity also influence absorption.

 

product-750-1120
product-750-1120
product-750-1120

 

Distribution: Lidocaine Hydrochloride Injection is distributed throughout total body water. Rapid disappearance (alpha phase) is related to uptake by highly perfused tissues. Slower distribution (beta phase) occurs in slowly equilibrating tissues, followed by metabolism and excretion (gamma phase). Lidocaine distributes less rapidly than prilocaine but similarly to mepivacaine. Skeletal muscle contains the highest percentage due to mass.

 

Biotransformation: Primarily metabolized in the liver, lidocaine undergoes oxidative de-ethylation to monoethylglycinexylidide, followed by hydrolysis to xylidine. Some degradation may occur in other tissues.

Elimination: Excretion primarily occurs via the kidneys, with less than 5% unchanged in urine. Renal clearance is inversely related to protein binding affinity and urine pH, suggesting non-ionic diffusion for lidocaine excretion.

 

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