Other Uses Of Lidocaine
Lidocaine is known to be one of the most commonly used local anesthetics. But what many people may not know is that lidocaine, as an anesthetic, also has many non-anesthetic effects, which are quite amazing. Lidocaine in addition to the anesthetic effect, its non-anesthetic effect also has more extensive application value, has a good application prospect, so it is worth us to further study, more widely explore the application of lidocaine and other local anesthetics.
The local anesthetic lidoca, as a sodium channel blocker, has membrane stability and is used against ventricular arrhythmias. In recent years, with the deepening of the pharmacological research and clinical application of lidocaine has the regulating function of the immune system and play anti-inflammatory effects in inflammatory reaction of multiple links, the significant inhibiting inflammatory reaction and acute lung injury, the sensitization effect of anti-cancer drugs, antibacterial, brain protection and reduce the postoperative cognitive dysfunction (POCD), and other aspects of the role is clinical scholar's attention.
1. Antibacterial activity of lidocaine
The antimicrobial activity of local anesthetics was first reported in 1909. Through the study of 1200 clinical bacterial specimens, some scholars found that lidocaine has different degrees of inhibition on staphylococcus aureus, Escherichia coli and other pathogenic bacteria and isolated fungi, and the inhibition rate increases with the increase of local anesthetic concentration, which can well prevent a variety of hospital infections. Some studies have shown that lidocaine and bupivacaine have significant bacteriostatic effect at common clinical doses (0.5% ~ 1.0% lidocaine and 0.125% ~ 0.25% bupivacaine), and the bacteriostatic effect tends to increase with the increase of concentration. In addition, 1% lidocaine had stronger antibacterial effect than 0.125% bupivacaine. It has been reported that lidocaine inhibits the adhesion and chemotaxis of granulocytes and has general cytotoxicity.
Studies have shown that local anesthetics inhibit cell growth of EScherichia coli, lead to outflow of cell contents and interfere with respiration. In conclusion, lidocaine is safe and feasible to prevent the growth of microorganisms in the epidural space and catheter during epidural anesthesia or prolonged postoperative analgesia. The mechanism of antibacterial activity of local anesthetics such as lidocaine is still unclear. It is possible that the interaction between local anesthetics and macromolecules on the surface of bacterial cells or cell membranes interferes with eukaryotic and prokaryotic cell membranes, changes the function of cell membranes, and leads to the death or growth inhibition of bacteria.
2. Brain protection of lidocaine
Lidocaine can easily cross the blood-brain barrier and has membrane stability. Under normal physiological conditions, the concentration of ion inside and outside the cell is relatively constant, and abnormal ion current may appear in brain cells during the early stage of ischemia and hypoxia. Studies have shown that lidocaine has a certain protective effect on brain. It is concluded that lidocaine can not only directly contract the large blood vessels in the brain and the whole body, but also dilate the cerebral microvessels at the site of trauma. The contraction of intracranial large blood vessels can rapidly reduce the intracranial pressure, and the relief of microcirculation spasm in the focal area can improve the blood supply of ischemic brain tissue without the suspicion of "stealing blood".
Studies have shown that intraoperative lidocaine in patients with supratentorial tumor resection can reduce brain oxygen metabolism, reduce anaerobic glycolysis, maintain blood glucose stability, do not prolong postoperative recovery time, play a role in brain protection, and can be safely used in brain surgery. The above studies have shown that lidocaine has a protective effect on brain, and its mechanism may be through blocking Na+, K+ and Ca2+ channels, reducing intracellular Na+ and Ca2+ concentration, reducing ATP consumption, protecting hypoxic nerve cells, reducing K+ outflow, inhibiting the release of excitatory amino acids and oxygen free radicals, and alleviating brain tissue damage. Improve cerebral blood flow and play a protective role in brain.
3. Anti-arrhythmic effect of lidocaine
Lidocaine has broad - spectrum anti - arrhythmic effect. Ventricular arrhythmias include ventricular premature systole, ventricular tachycardia, ventricular flutter and ventricular fibrillation. The latter three are known as malignant arrhythmias, which are one of the independent risk factors for sudden cardiac death. Malignant ventricular arrhythmias often lead to hemodynamic deterioration, accelerate the progression of the disease, and even endanger life.
Because of IB class of antiarrhythmic drugs, lidoca selectively acts on purkinje fibrocytes and ventricular myocytes, which can slow down the 4-phase depolarization rate, reduce purkinje fibroself-discipline, promote K+ outflow and shorten the action potential duration, and relatively prolong the effective refractory period. It is often used for the prevention and treatment of ventricular arrhythmia. Lidocaine can slow down the conduction function of the heart, inhibit cardiac contractility and reduce cardiac output. Lidocaine has been used in clinical anti-arrhythmia for a long time and has more experience. In the face of ventricular arrhythmia, clinicians often choose lidocaine for control, which has high effectiveness and safety.
4. Lidocaine can prevent excessive inflammation
Many studies have shown that lidocaine is effective in preventing and controlling traumatic or endotoxin-induced inflammatory reactions. Lidocaine is a membrane stabilizer that inhibits the adhesion and aggregation of neutrophils (PMN), reduces the release of oxygen free radicals and proteolytic enzymes, stabilizes cell membranes, regulates cytokines, and inhibits excessive inflammatory responses. Inflammatory mediators LB4 and INTERleukin 1α (IL-1α) are strong PMN chemoattractants, inducing PMN binding, desorption, exudation, superoxide generation, and synergistic with prostaglanin E2 to increase vascular permeability.
With mononuclear cells in vitro with different concentrations (2 ~ 20 mol/L) lidocaine can significantly inhibit LB4 incubation, IL - 1 alpha release, a mole of lidocaine concentrations can inhibit the white blood cells, mast cells, basophils release of histamine, that lidocaine can inhibit some of the key of the release of inflammatory mediators and anti-inflammatory effect.
In clinical application, a number of studies have found that intraoperative intravenous infusion of lidocaine can regulate the immune function of patients and accelerate their postoperative recovery. Herroeder is equivalent to intraoperative lidocaine infusion in patients undergoing colorectal surgery. The results showed that perioperative intravenous lidocaine infusion could accelerate the recovery of enhanced gastrointestinal function and significantly shorten the length of hospital stay. Meanwhile, intravenous lidocaine infusion could significantly reduce the expression levels of IL-6, IL-8, complement C3a, CD-11b, etc. The mechanism may be the anti-inflammatory effect of lidocaine on surgical trauma.
It has been reported that in a prospective randomized double-blind controlled trial, intravenous lidocaine infusion was given to out-patient laparoscopic patients, and it was found that the postoperative recovery index of patients in the lidocaine group was significantly improved, and intravenous lidocaine infusion could significantly shorten the length of hospital stay, and the opioid dose of patients was also significantly reduced. In the process of PCIA, there are complications such as phlebitis. Adding lidocaine into the intravenous analgesic pump can effectively prevent the occurrence of phlebitis.
It may be that lidocaine acts on vascular endothelial cells and peripheral nerve receptors near the puncture point of vein, which dilates the blood vessels and inhibits the stimulation response of venous wall to trocar and the release of inflammatory factors of vascular endothelial cells. Dilated blood vessels speed up blood flow and prevent platelets from gathering, thus preventing the formation of microthrombus and phlebitis. Chemotherapy-induced phlebitis often occurs in clinic. Studies have shown that intravenous infusion of low-dose lidocaine plus dexamethasone is effective in preventing chemotherapy-induced phlebitis.
Anyhow, perioperative small dose of lidocaine intravenous injection can reduce operation caused by inflammation, reduce the surgery, a kind of commonly used local anesthetics amide class, studies have shown that it has anti-inflammatory effects, and perioperative intravenous lidocaine can reduce postoperative pain, reduce opioid use, reduce the body's inflammatory response, accelerate gastrointestinal function recovery and shorten hospitalization time. Further study on the protective effect and mechanism of lidocaine on the immune function decline caused by surgical trauma can provide a new theoretical basis for the application of lidocaine in clinical anti-inflammatory treatment.
5. Application of lidocaine in acute lung injury
Acute lung injury (ALI) is the injury of alveolar epithelium and vascular endothelial cells caused by inflammatory reactions in the lung caused by various factors other than cardiogenic. Its pathogenic mechanism is the expression of excessive and uncontrolled systemic inflammatory response in the lungs. The underlying pathophysiology is an uncontrolled inflammatory response centered on infiltration of PMN and pulmonary microvascular damage. Under normal circumstances, PMN exudation and removal of necrotic tissue is a normal response of the body to resist foreign invasion. Under the precise regulation of the body, the inflammatory response is limited to local areas, but when the infection is serious, the regulatory mechanism is destroyed, and PMN activation is out of control, leading to the expansion of the inflammatory response.
Many experimental studies have confirmed that lidocaine can inhibit the inflammatory response of PMN and reduce acute lung injury caused by various causes. In the lung injury model, intravenous lidocaine pretreatment significantly improved airway dynamics, oxygenation, pulmonary vascular permeability, histopathological changes, and biochemical changes of alveolar lavage fluid compared with untreated patients. In conclusion, lidocaine can stabilize cell membrane, act on PMN, participate in all links of inflammatory reaction, inhibit PMN migration to injured tissue, metabolism and adhesion to endothelial cells, thus reducing a variety of causes.
