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The administration of drugs multi slim yousi negativ neuroprotective effect should be considered in order to reduce the risk of cerebral palsy after severe preterm birth. Magnesium sulfate MgSO4the objective of this analysis, has been proposed as an important part of the management of unavoidable preterm birth for the prevention of cerebral palsy and neonatal death. The beneficial effects of this inexpensive and simple treatment are observed regardless of the reason for preterm birth, with similar results on different premature gestational ages.
MgSO4 has been shown to have multi slim yousi negativ neuroprotective effect by reducing brain metabolism and has also a beneficial hemodynamic effect by stabilizing blood pressure, reducing constriction in the cerebral arteries, and restoring infusion in preterm infants.
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If the birth did not occur after 12 hours and is no longer considered imminent birth, the infusion stops and resumes in case of recurrence of the imminent birth. Both protocols are demonstrated to be efficient, with no maternal side effects.
Keywords MgSO4, neuroprotection, fetal, cerebral palsy Rezumat Profilaxia deficienţei neurologice a nou-născuţilor prematuri rămâne o provocare pentru neonatologi. Administrarea medicamentelor cu efect neuroprotector trebuie luată în considerare pentru a reduce riscul de paralizie cerebrală după naşterea prematură severă.
Sulfatul de magneziu MgSO4obiectivul acestei analize, a fost propus ca parte importantă a managementului naşterii premature inevitabile pentru prevenirea paraliziei cerebrale şi a morţii neonatale. Efectele benefice ale acestui tratament ieftin şi simplu sunt observate indiferent de motivul naşterii premature, dieta de slabit pentru cardiaci rezultate similare la diferite vârste de gestaţie premature.
S-a dovedit că MgSO4 are un efect neuroprotector prin reducerea metabolismului creierului şi, de asemenea, are efecte hemodinamice benefice prin stabilizarea tensiunii arteriale, reducerea constricţiei în arterele cerebrale şi restabilirea circulaţiei cerebrale la copiii prematuri.
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Există două regimuri standard propuse. Dacă naşterea nu a avut loc după 12 ore şi nu mai este considerată naştere iminentă, perfuzia se opreşte şi se reia în caz de reapariţie a riscului de naştere iminentă. Ambele protocoale sunt dovedite a fi eficiente, fără efecte secundare materne.
The mechanisms involved can imply both inflammation and ischemic injury. Other causes of CP include: fetal anemia, intrauterine transfusions, or fetal alcohol syndrome 4,5. However, preterm birth remains the most important risk factor 3. In some countries, the incidence of CP has increased in recent years due to improved medical care of the small premature infants, thus increasing their survival rate, but not their neurological prognosis 7.
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Various studies associate severe intraventricular hemorrhage and periventricular leukomalacia with CP 8. The cerebral vascular anatomy prior to week 32 of gestation consists of two systems with no anastomoses between them: multi slim yousi negativ ventriculopetally system which irrigates the cortex and the ventriculofugal system it descends to the ventricles. The area between these two systems is vulnerable to ischemia.
Due to the fact that through this area pass the pyramidal tracts, an ischemic lesion at this level may cause spastic diplegia 9. After 32 GWs, the cerebral blood flow is oriented towards the cortex. Therefore, hypoxic lesions occurring after this age will primarily affect the cortical regions of the brain. Other studies claim that fetal infection may be an important element in the relationship between preterm birth and CP Antenatal infection of the genitourinary tract determines the production of proinflammatory cytokines IL1, IL6, IL8, TNF that stimulate prostaglandin production and induce preterm labor The same cytokines have also direct toxic effects on oligodendrocytes and myelin Vascular rupture, tissue hypoxia, and cytokine-mediated destructions determine a massive neuronal apoptosis.
As a consequence, the released glutamate acts upon membranar receptors, allowing the influx of calcium into the neurons cytoplasm. Intracellular hypercalcemia itself has a toxic effect upon white matter. Moreover, glutamate has a direct toxic action on oligodendrocytes Therefore, prospective research has been conducted in order to identify a potential profilactic drug with neuroprotective effect that can reduce the risk of neurodevelopmental disorders of preterms, magnesium sulfate MgSO4 studies being promising In term of cell biology, neuroprotection translates the inhibition of the biochemical response to ischemia in order to prevent neuronal death.
The role and distribution of magnesium in the human body Magnesium is the fourth most widespread ion in the body and contributes to several physiological processes, including cellular and energetic metabolism Within the human brain, magnesium is mainly linked to chelators such as adenosine triphosphate Multi slim yousi negativ and is a cofactor in more than enzymatic reactions.
Magnesium also contributes to glycolysis and ATP production, acting as a membranar cell stabilizer In the central nervous system, magnesium acts as a non-competitive blocker of N-methyl-D-aspartate NMDA glutamate receptor, modulating calcium influx and preventing excitotoxic injury caused by it. In ischemic conditions, the level of extracellular glutamate decreases, possibly reducing excitotoxicity Magnesium limits calcium influx through voltage-dependent channels, which may reduce apoptosis activation Magnesium has also intrinsic anti-inflammatory properties, reducing both oxidative stress and the production of pro-inflammatory cytokines: interleukin-6 IL6 and tumor necrosis factor-a TNF-a Magnesium deficiency increases the production of endothelial nitric oxide, which can promote endothelial dysfunction.
The exact pathways involved are multiple: decreased calcium influx and phagocyte cell activation, inhibition of neurotransmitter release, or inhibition of nuclear factor kappa B.
Its physiological role as a calcium channel blocker and modulator of sodium and potassium flux through its action on ion pumps e. The normal concentration of magnesium in adult plasma is 0.
Prevenirea paraliziei cerebrale la sugarii prematuri - rolul potenţial al sulfatului de magneziu
In newborns, magnesium concentrations increases in the first week after birth 0. In animals, the concentration of magnesium in fetal blood increases after maternal administration and has a positive correlation with maternal blood levels The neuroprotective effects of MgSO4 demonstrated in preclinical studies Multi slim yousi negativanimal studies have been conducted to investigate the neuroprotective role of magnesium.
Early experiments involved adult animal models. InVacanti and Ames demonstrated the neuroprotective effects of MgSO4 in a model of ischemia of the spinal cord in rabbits Inthe administration of MgSO4 to rat hippocampal slices reduced the effect of hypoxia McIntosh et al.
Several studies have reported the importance of intraperitoneal administration of MgSO4 in reducing excitotoxic brain injury in mice, lesions induced by intracerebral injection of ibotenate a glutamate receptor agonist These effects ultimately prevented programmed cell death The neuroprotective effect of MgSO4 was also evaluated under inflammatory conditions.
In multi slim yousi negativ hypoxic-ischemic injury model, in vitro, MgSO4 was involved in the protection of oligodendrocytes