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1 Magnesium ion calcium channel blockade 1.1 Controlled hypotensive magnesium ion blocks calcium ion channels, inhibits calcium ions from entering the vascular endothelial cells, and dilates blood vessels; while reducing the sensitivity of vascular tissue to sympathomimetic adrenergic responses, The sympathetic ganglia impaired impulse transmission, thereby expanding blood vessels. In cardiopulmonary bypass, magnesium has been shown to be as effective as nicardipine in controlling arterial pressure and reducing systemic vascular resistance. Blood loss can be reduced by reducing arterial blood pressure, but cardiac output should not be reduced because stable cardiac output is important for maintaining tissue blood flow. Nakaigawa et al. demonstrated in animal experiments that intravenous administration of magnesium resulted in dose-dependent arterial blood pressure, heart rate, left ventricular per cent work index (LVMWI), coronary perfusion pressure (CPP), coronary vascular resistance, and myocardial oxygen consumption ( MVO2) decreases but maintains cardiac output well. Second, despite the decrease in coronary perfusion pressure, coronary vascular resistance did not change at the same time, so coronary sinus blood flow did not change, suggesting that magnesium may have coronary vasodilation.
1.2 Anticonvulsants and Prevention of Local Anesthetic Poisoning Magnesium is widely used in obstetrics as an anticontractor. The anticonvulsant effect of magnesium ions is to expand the cerebrovascular vasospasm and reduce the cerebral perfusion pressure (CPP), because magnesium is a central calcium antagonist; it also antagonizes N-methyl-D-aspartate (NMDA) The receptor increases the production of vasodilator prostaglandins and dilates the cerebral arteries; it may also inhibit seizures due to the membrane stabilization of magnesium. In recent years, studies have shown that intravenous injection of magnesium sulfate 50 mg?kg-1 before neck or brachial plexus block or fistula block can effectively prevent the local anesthetic toxicity reaction. The concentration of Mg2+ in the extracellular fluid increases the central nervous system. Inhibition, resulting in anticonvulsant and sedative effects, have a significant effect on the prevention of local anesthetic toxicity, especially the reduction of convulsions.
1.3 Neuromuscular Relaxation The role of magnesium ions in enhancing calcium channel blockade and prolonging the effects of non-depolarizing muscle relaxants has been relatively clear. Some animal experiments show that magnesium ion enhances the muscle relaxant effect of depolarizing muscle relaxant succinylcholine, but it has not been supported in clinical observation. The change of magnesium ion concentration does not change the muscle relaxation characteristics of succinylcholine. Sakuraba et al. compared preconditioning with magnesium and pretreatment with vecuronium before rapid sequential induction of tracheal intubation. The results showed that the former can more effectively reduce succinylcholine-induced tremor and hemodynamic instability. Adverse reactions, but can not avoid increased potassium concentration after induction.
1.4 Treatment of postoperative chills studies have shown that the ratio of calcium to sodium ion concentration determines the set point of body temperature. Animal experiments have shown that elevated calcium concentration can cause a decrease in body temperature. Magnesium ion is a physiological antagonist of calcium channels and prevents the influx of calcium ions. This prevents the body temperature from falling. Norepinephrine and serotonin have the effect of regulating body temperature. Magnesium is an NMDA receptor antagonist. NMDA regulates body temperature by regulating the activity of norepinephrine and serotonergic neurons. Therefore, it can be used as a good input source of thermal information, stimulating the body temperature regulation center, reducing the chill response and reducing the occurrence of chills. After intravenous administration to magnesium, the patient can produce a transient systemic fever sensation, stimulate the body temperature regulation center, and reduce the chill response threshold, thereby inhibiting the occurrence of chills.
1.5 The mechanism of expansion of bronchial magnesium by expanding bronchioles and improving lung function may be: (1) magnesium ions reduce intracellular calcium ion concentration, relieve airway smooth muscle spasm and make bronchiectasis; (2) magnesium ions activate adenosine on cell membrane Acid cyclase promotes ATP production of cAMP, cAMP / cGMP ratio, and through the activation of protein kinase and ATP enzyme, stabilize the membrane potential, prevent the release of allergic substances, thereby eliminating airway spasm, improve the state of hypoxia, and improve the pulmonary circulation; (3) Magnesium ions reduce the release of acetylcholine from the motor nerve endings, counteract the stimulatory action of acetylcholine on smooth muscle cells, directly relieve smooth muscle spasm and improve lung ventilation and ventilation; (4) Magnesium ions up-regulate the number of β2 receptors, Increase the airway mucosal epithelial β2 receptor affinity, improve the lower β2 receptor function in asthma patients, thereby exerting bronchodilation effect.
1.6 Intracellular calcium overloading is one of the important mechanisms of ischemia-reperfusion (IR) injury. In vitro cardiac perfusion tests show that high concentrations of magnesium salt (15 mol?L-1) can effectively protect Ca 2+ - The activity of ATPase facilitates the synthesis of mitochondrial ATP and reduces calcium overload, suggesting that high concentrations of magnesium perfusate can partially reverse myocardial IR injury.
After cerebral ischemia, serum magnesium levels will decrease and have a positive correlation with the extent of brain function impairment. Low magnesium ions can increase calcium overload, cause accumulation of excitatory amino acids and increase brain damage. A sufficient amount of magnesium is the precondition for ATP regeneration after ischemia-reperfusion. Magnesium is also an NMDA receptor blocker and excitatory amino acid inhibitor, which can inhibit the activation of glutamate receptors and relieve astrocyte edema. Maintain the integrity of the blood-brain barrier.
Spinal motoneurons are extremely sensitive to short ischemia and may even cause paraplegia. Studies have confirmed that intrathecal injection of magnesium can prevent spinal cord ischemic injury caused by thoracoabdominal aorta blockade. Mg2+ acts as a Ca2+-mediated NMDA inhibitor in the absence of After the blood injury acts as a neuroprotein, extracellular high magnesium concentration can significantly inhibit the release of the excitatory neurotransmitter glutamate in the cerebrospinal fluid and inhibit its receptors, which reduces the ischemic lesions in the acute phase of the lumbar 3-lumbar 6 The death of the motor neuron at the focal point significantly increased the motor function of the lower extremities and delayed the degeneration and death of neurons around the focus of the (thoracic 7-lumbar 2) lesion.
In recent years, the protective effect of magnesium on erythrocytes has also been studied. It has been found that the erythrocyte membrane Ca2+-ATPase in preeclampsia mothers is reduced to about 50% of normal pregnant women, and calcium overload and glutathione synthesis are reduced in erythrocytes. A series of oxygen free radicals are initiated, and the lipid peroxidation damage of the erythrocyte membrane is enhanced. Abad et al. treated 11 patients with severe preeclampsia by intravenous injection of magnesium (4 g of MgSO4 was given as a loading dose intravenously within 30 minutes, followed by a maintenance dose of 1 g?h-1), and treated with magnesium for 24 hours. Ca2+-ATPase activity increased, lipid peroxidation injury decreased, and there was an inverse correlation between the two, and there was no difference compared with normal pregnant women. The use of magnesium for the treatment of intrauterine distress in neonates (intravenous injection of magnesium at 250 mg?kg-1 within 2 hours of injection with an injection time of 30 minutes) also led to the same conclusion. Compared with normal controls, patients with essential hypertension have decreased Na+, K+-ATPase, Ca2+, Mg2+-ATPase activity, and Mg2+ content in erythrocytes, and elevated intracellular Ca2+ content; mean arterial pressure and Na+ There was a negative correlation between K+-ATPase and Ca2+, Mg2+-ATPase activity, and a positive correlation with Ca2+ in erythrocytes. There was a positive correlation between erythrocyte ATP content and Mg2+ content in red blood cells. This indicates that the occurrence of hypertension is related to the abnormal transport of plasma membrane ion, which is closely related to the increase of intracellular Ca2+ and the decrease of Mg2+.
2 Magnesium NMDA receptor antagonism 2.1 Prevention of cardiovascular adverse reactions during endotracheal intubation Stimulation of tracheal intubation is related to the release of catecholamines. Magnesium ions antagonize NMDA receptors in the central nervous system and reduce peripheral nociceptors sensitization. The effect is to reduce the release of catecholamines and weaken a series of cardiovascular reactions such as increased heart rate and high blood pressure that may be associated with tracheal intubation. Altan et al. were treated with magnesium, clonidine, and placebo before tracheal intubation, and the results were in the magnesium sulfate group (IV 50 mg?kg-1 before induction of general anesthesia; continuous infusion of 10 mg?kg-1?h during the operation. -1) Mean arterial pressure and heart rate were reduced after induction of anesthesia and during surgery, and propofol consumption was also significantly reduced during anesthesia induction and surgery maintenance.
2.2 Perioperative analgesia The analgesic mechanism of magnesium ions may be through the action of NMDA receptors in the central nervous system, reducing the sensitivity of the central nervous system to pain and inhibiting the spinal cord's facilitation of pain stimuli; Ions can act on peripheral NMDA receptors and calcium channels, and may even have magnesium channels, thereby producing direct analgesia and reducing the sensitivity of the peripheral nervous system to noxious stimuli, affecting the sympathetic nervous system, and reducing catecholamines. The release of neurotransmitters.
2.2.1 Intravenous Infusion of Magnesium Perioperative Analgesia Ryu et al. performed total intravenous anaesthesia in 55 patients undergoing gynecological surgery, intravenous magnesium sulfate (50 mg?kg-1) before induction of anesthesia, and continuous magnesium infusion during surgery. The agent (15 mg?kg-1?h-1) was given to the magnesium group in terms of postoperative pain scores, cumulative postoperative morphine requirements, and incidence of chills compared with the same amount of placebo before and after induction of anesthesia and intraoperative intravenous administration. The dose of rocuronium in the operation was significantly lower than placebo. Anbarci evaluated 70 patients with brachial plexus block using a randomized, double-blind method to assess the perioperative analgesic effect of magnesium during the magnesium sulfate group (5 mg?kg-1 postoperatively and 500 mg?h-1 within 24 hours). Note) Compared with the control group, the cumulative analgesic requirement and VAS score were significantly reduced.
In addition, intravenous administration of magnesium significantly reduced pain when propofol and rocuronium were injected. Aygun et al. pretreated with magnesium sulfate and ketamine before induction of general etomidate induction showed that the magnesium group (2.48) Mmol IV) decreased the degree of pain caused by etomidate and the incidence and intensity of myoclonus, while the ketamine group could not effectively reduce the incidence and intensity of myoclonus.
2.2.2 Epidural or subarachnoid administration of magnesium for perioperative analgesia Bilir et al. on 55 patients undergoing hip joint surgery under hard-waist joint anesthesia followed by fentanyl or magnesium alone with fentanyl The results of epidural analgesia (PCEA) were compared. The results showed that the use of epidural fentanyl, 24 h postoperative fentanyl and VAS scores in the posterior group were all significantly lower than those in the former group, suggesting that magnesium adjuvanted opioids Analgesics are effective and safe for PCEA. Buvanendran et al. demonstrated that anesthesia in the subarachnoid space (50 mg) can significantly prolong the analgesic effect of fentanyl in labor-induced analgesia.
2.2.3 Use of Magnesium in Venous Local Anesthesia Turan et al. demonstrated that patients undergoing elective hand surgery under venous local anesthesia demonstrated that magnesium ions as an adjunct to lidocaine can significantly reduce postoperative analgesics during intravenous local anesthesia The consumption and reduction of pain in the tourniquet, shortening the onset time of sensory and motor block, prolonging the recovery time and the time needed for the first postoperative analgesic can improve the analgesic quality of intravenous and local anesthesia.
2.2.4 Intra-articular injection of magnesium for perioperative analgesia Bandok et al. At the end of arthroscopic surgery, intra-articular injection of 10 mL of magnesium sulfate (50 mg?mL-1) to the patient resulted in 1, 2, 6 postoperatively. The 8 h pain simulation score and 24 h postoperative analgesic requirement were significantly lower than those in the placebo group in which 10 mL of 0.9% sodium chloride solution was intraarticularly injected.
3 Membrane stabilization of magnesium ions Magnesium ions activate Na+-K + ATPase and cardiac adenylyl cyclase, and play an important role in maintaining the integrity of myocardial mitochondria and promoting their oxidative phosphorylation. To reduce the loss of intracellular potassium in digitalis poisoning, anti-arrhythmia effect. One study showed that intravenous administration of magnesium can reduce the incidence of post-coronary atrial fibrillation (POAF) and decrease hospital stay (LOS). Compared with intraoperative and postoperative prophylactic administration of magnesium, preoperative administration significantly reduced the incidence of POAF; compared to moderate and high doses of magnesium, low doses of magnesium were administered (average cumulative dose of 8.2 g, dose Range 6.5 to 9 g) The incidence of POAF is lower.
Magnesium Application in Medicine