1 calcium channel blocking effect of magnesium ion
1.1 Controlled buck
Magnesium ions block calcium channels, inhibit calcium ions from entering vascular endothelial cells, and dilate blood vessels. At the same time, they reduce the sensitivity of vascular tissues to sympathetic adrenergic substances, and cause sympathetic ganglion impulse transmission, thereby expanding blood vessels. In cardiopulmonary bypass, magnesium has been shown to control arterial pressure as effectively as nicardipine and reduce systemic vascular resistance. Blood loss can be reduced by lowering arterial blood pressure, but cardiac output should not be reduced because stable cardiac output is important for maintaining tissue blood perfusion. Nakaigawa et al. demonstrated in animal experiments that intravenous magnesium injection resulted in dose-dependent arterial blood pressure, heart rate, left ventricular labor index (LVMWI), coronary perfusion pressure (CPP), coronary vascular resistance, and myocardial oxygen consumption ( MVO2) is lowered, but the cardiac output is well maintained. Secondly, although the coronary perfusion pressure is reduced, the coronary vascular resistance is also reduced, so there is no change in coronary sinus blood flow, suggesting that magnesium may have coronary relaxation.
1.2 Anticonvulsing and prevention of local anesthetic poisoning
Magnesium is widely used in obstetrics as an anti-uterine drug. The anticonvulsant effect of magnesium ions is to dilate the cerebral blood vessels of the sputum and reduce the cerebral perfusion pressure (CPP), which is because the magnesium agent is a central calcium antagonist; it also antagonizes N-methyl-D-aspartate (NMDA). The receptor increases the production of the vasodilator prostaglandin and dilates the cerebral artery; it may also inhibit the occurrence of convulsions due to the membrane stabilization of the magnesium agent. In recent years, studies have shown that intravenous injection of magnesium sulfate 50 mg?kg-1 before neck, brachial plexus block or fistula block can effectively prevent local anesthetic toxicity, and increase the concentration of Mg2+ in extracellular fluid to cause central nervous system. Inhibition, anticonvulsant and sedative effects have a significant effect on preventing local anesthetic toxicity, especially reducing convulsions.
1.3 neuromuscular relaxation
The role of magnesium ions in enhancing calcium channel blockage and prolonging the role of non-depolarizing muscle relaxants has become clear. Some animal experiments have shown that magnesium ion enhances the muscle relaxant effect of depolarizing muscle relaxant succinylcholine, but it is not supported in clinical observation. The change of magnesium ion concentration does not change the muscle relaxant characteristics of succinylcholine. Sakuraba et al. compared magnesium pretreatment with pretreatment with vecuronium prior to rapid sequential induction of tracheal intubation, and found that the former can more effectively reduce sib choline-induced fasciculation and hemodynamic instability. Adverse reactions, but can not avoid the increase of serum potassium concentration after induction.
1.4 treatment of postoperative shiver
Studies have shown that the ratio of calcium to sodium ion concentration determines the body temperature setting point. Animal experiments show that elevated calcium ion concentration can cause body temperature to drop, magnesium ion is a physiological antagonist of calcium channel, preventing calcium ion influx and preventing body temperature drop. Norepinephrine and serotonin regulate body temperature. Magnesium ion is an NMDA receptor antagonist. NMDA regulates body temperature by regulating the activity of norepinephrine and serotonergic neuron. Therefore, it can be used as a good source of thermal information input, stimulate the body temperature regulation center, reduce the cold war response, and reduce the occurrence of chills. After intravenous administration of magnesium, the patient can develop a transient systemic fever, stimulate the body temperature regulation center, and reduce the threshold of shivering response, thereby suppressing the occurrence of shivering.
1.5 expansion of the bronchi
The mechanism by which magnesium can expand the bronchus and improve lung function may be: (1) magnesium ion reduces intracellular calcium ion concentration, relieves airway smooth muscle spasm, and causes bronchiectasis; (2) magnesium ion activates adenylate cyclization on cell membrane Enzymes promote the production of cAMP by ATP, increase the cAMP / cGMP ratio, and stabilize the membrane potential by activating protein kinase and ATPase to prevent the release of allergic substances, thereby releasing airway spasm, improving hypoxia and improving pulmonary circulation; (3) Magnesium ions reduce the release of acetylcholine from motor nerve endings, resist the stimulating effect of acetylcholine on smooth muscle cells, directly relieve smooth muscle spasm, improve lung ventilation and ventilation function; (4) magnesium ions increase airway by up-regulating the number of β2 receptors Mucosal epithelial β2 receptor affinity enhances the hypothetical β2 receptor function in asthmatic patients, thereby exerting a bronchodilator effect.
1.6 Reduce intracellular calcium overload
Calcium overload is one of the important mechanisms of ischemia-reperfusion (IR) injury. In the isolated heart perfusion test, high concentration of magnesium salt (15 mol? L-1) can effectively protect Ca 2+ -ATPase activity. Conducive to the synthesis of mitochondrial ATP, reducing calcium overload, suggesting that high concentration of magnesium perfusate can partially reverse myocardial IR damage.
Serum magnesium levels are reduced after cerebral ischemia and are positively correlated with the extent of brain damage. Low magnesium ions can increase calcium overload, leading to the accumulation of excitatory amino acids and aggravate brain damage. A sufficient amount of magnesium is a prerequisite for ATP regeneration after ischemia-reperfusion. Magnesium ions are also NMDA receptor blockers and excitatory amino acid inhibitors, which inhibit the activation of glutamate receptors and alleviate astrocyte edema. Maintain the integrity of the blood-brain barrier.
Spinal motor neurons are extremely sensitive to short ischemia and may even cause paraplegia. Studies have shown that intrathecal magnesium can prevent spinal cord ischemic injury caused by thoracic and abdominal aortic occlusion, and Mg2+ is a Ca2+-mediated NMDA inhibitor. After blood damage, it acts as a neuroprotein. Extracellular high magnesium concentration can significantly inhibit the release of excitatory neurotransmitter glutamate and inhibit its receptor in cerebrospinal fluid, which reduces (lumbar 3-lumbar 6) acute ischemic injury lesions. The focus of motor neuron death significantly increased motor function in the lower extremities, while delaying neuronal degeneration and death around the focus of the chest (thorax 7-lumbar 2).
In recent years, the protective effect of magnesium on red blood cells has also been studied. It is found that the erythrocyte membrane Ca2+-ATPase in premature eclampsia is reduced to about 50% of normal pregnant women, calcium overload in red blood cells and glutathione synthesis are reduced. A series of oxygen free radicals are triggered, and the lipid peroxidation damage of the red blood cell membrane is enhanced. Abad et al. treated 11 patients with severe pre-eclampsia with intravenous magnesium (4 g MgSO4 as a loading dose within 30 min, followed by 1 g?h-1 as a maintenance dose), and treated with magnesium for 24 h after erythrocyte membrane Ca2+-ATPase activity increased, lipid peroxidation damage decreased, and the two were inversely correlated, and there was no difference compared with normal pregnant women. Neonates treated with magnesium in the treatment of intrauterine distress (intravenous magnesium 250 mg? kg-1 within 2 hours of delivery, 30 min injection time) also reached a consistent conclusion. Compared with normal controls, erythrocyte membrane Na+, K+-ATPase, Ca2+, Mg2+-ATPase activity and erythrocyte Mg2+ content decreased, and erythrocyte Ca2+ content increased. Mean arterial pressure and Na+ were found in patients with essential hypertension. K+-ATPase was negatively correlated with Ca2+ and Mg2+-ATPase activities, and positively correlated with Ca2+ in red blood cells. ATP content in red blood cells was positively correlated with Mg2+ content in red blood cells. It is indicated that the occurrence of hypertension and the active transport of cell membrane ions are related to the increase of intracellular Ca2+ level and the decrease of Mg2+.
2 Magnesium ion NMDA receptor antagonism
2.1 Prevention of cardiovascular adverse reactions during endotracheal intubation
Stimulation of tracheal intubation is associated with the release of catecholamines, which antagonize NMDA receptors in the central nervous system, reduce peripheral nociceptor sensitization, reduce catecholamine release, and impair heart rate that may be associated with tracheal intubation A series of cardiovascular reactions such as elevated blood pressure. Altan et al. pretreated with magnesium, clonidine, and placebo before endotracheal intubation. 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 surgery). -1) The mean arterial pressure and heart rate decreased after induction of anesthesia and during surgery, and the consumption of propofol was also significantly reduced during anesthesia induction and maintenance.
2.2 perioperative analgesic effect
The analgesic mechanism of magnesium ion 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 facilitation of spinal cord on pain stimuli; while magnesium ions can act on peripheral NMDA Receptors and calcium channels, and possibly even magnesium channels, produce direct analgesic effects and reduce the sensitivity of the peripheral nervous system to noxious stimuli, affect the sympathetic nervous system, and reduce the release of catecholamines and neurotransmitters.
2.2.1 Intravenous infusion of magnesium agent perioperative analgesia Ryu et al. performed total intravenous anesthesia in 55 patients undergoing gynecological surgery, prior to induction of intravenous anesthesia with magnesium sulfate (50 mg? kg-1) and continuous infusion of magnesium during surgery. The dose (15 mg?kg-1?h-1) compared with the same amount of placebo before and during anesthesia induction, the postoperative pain score of the magnesium group, the cumulative morphine requirement after surgery, the incidence of chills and The amount of rocuronium used in the operation was significantly lower than that of placebo. Anbarci evaluated the perioperative analgesia of magnesium in 70 patients with brachial plexus block by randomized double-blind method. Magnesium sulfate group (5 mg?kg-1, 500 mg?h-1 within 24 h after surgery) Note) Compared with the control group, the cumulative analgesic requirement and VAS score were significantly lower.
In addition, intravenous administration of magnesium significantly reduced the pain when propofol and rocuronium were injected. Aygun et al. pretreated with magnesium sulfate and chloralkonium chloride before induction of etomidate, and the results showed magnesium group (2.48). Methyl IV) reduced the degree of pain caused by etomidate and the incidence and intensity of myoclonus, while the group of chloramphenicol did not effectively reduce the incidence and intensity of myoclonus.
2.2.2 Perioperative analgesia with magnesium in the epidural or subarachnoid space
Bilir et al compared the effects of fentanyl or magnesium combined with fentanyl for epidural analgesia (PCEA) in 55 patients undergoing hip surgery under combined spinal anesthesia. The results showed that the latter group was hard. The dose of fentanyl outside the membrane, total fentanyl and VAS scores at 24 h after surgery were significantly lower than those in the former group, suggesting that magnesium-assisted opioid analgesics are effective and safe for PCEA. Buvanendran et al. confirmed that the subarachnoid administration of magnesium (50 mg) significantly prolonged the analgesic effect of fentanyl in women who gave birth to analgesia.
2.2.3 Application of magnesium in local anesthesia of vein
In patients undergoing elective hand surgery under local anesthesia with intravenous anesthesia, Turan et al. demonstrated that magnesium ion as an adjunct to lidocaine during local anesthesia can significantly reduce postoperative analgesic consumption and reduce tourniquet pain and shorten The onset time of sensory and motor block, prolonging the recovery time and the time required for the first postoperative analgesic, can improve the quality of analgesia with intravenous plus local anesthesia.
2.2.4 intra-articular injection of magnesium perioperative analgesia
At the end of the arthroscopic surgery, Bondok et al. injected 10 mL of magnesium sulfate (50 mg?mL-1) into the patient. The results showed pain simulation scores at 1, 2, 6 and 8 h after surgery and 24 h postoperative analgesia. The drug requirements were significantly lower than the placebo group injected with 10 mL of 0.9% sodium chloride solution intra-articularly.
3 Membrane stabilization of magnesium ions
Magnesium ions activate Na+-K + ATPase and adenosine cyclase, which play an important role in maintaining myocardial mitochondrial integrity and promoting oxidative phosphorylation. It can reduce the loss of potassium ions in the cells when digitalis poisoning, and has anti-arrhythmia effect. One study showed that intravenous administration of magnesium reduced the incidence of postoperative atrial fibrillation (POAF) and reduced hospital stay (LOS) during coronary artery bypass grafting. Compared with intraoperative and postoperative prophylactic administration of magnesium, preoperative administration can significantly reduce the incidence of POAF; compared with medium and high doses of magnesium, low doses of magnesium (average cumulative dose of 8.2 g, dose) Range 6.5~9 g) The incidence of POAF is lower.
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Label: magnesium ion stabilization
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