Magnesium sulfate therapy after aneurysmal subarachnoid hemorrhage

Veyna, Richard S; Seyfried, Donald; Burke, Don G; Zimmerman, Chris; Mlynarek, Mark; Nichols, Victoria; Marrocco, Anna; Thomas, Ajith J.; Mitsias, Panayiotis; Malik, Ghiaus M

doi:10.3171/jns.2002.96.3.0510

Cited by 185 publications

(96 citation statements)

References 17 publications

(26 reference statements)

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“…24,26) However, recent prospective studies of continuous intravenous administration of magnesium sulfate in patients with aneurysmal SAH failed to show any vasodilatory effect on vasospasm detected by angiography and transcranial Doppler ultrasonography. 20,23) The blood-brain barrier is relatively impermeable to magnesium ion (Mg 2＋ ), so increased blood concentration of Mg 2＋ may not affect…”

Section: Introductionmentioning

confidence: 99%

Initial Clinical Experience of Vasodilatory Effect of Intra-cisternal Infusion of Magnesium Sulfate for the Treatment of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Mori

Yamamoto

Nakao

et al. 2009

Neurol. Med. Chir.(Tokyo)

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The vasodilatory effect of intra-cisternal infusion of magnesium sulfate solution was evaluated in 10 patients with symptomatic vasospasm after aneurysmal subarachnoid hemorrhage (SAH) who underwent early clipping surgery. Cisternal drainage was installed in the prepontine and/or sylvian fissures. Carotid angiography was performed immediately after the onset of symptomatic vasospasm, then intracisternal infusion of 15 mmol/l magnesium sulfate in Ringer solution was started at 20 ml/hr and continued until day 14. Irrigation was performed from the cisternal tube (inlet) to the spinal drainage (outlet). The cerebrospinal fluid magnesium ion concentration (1.2 ± 0.2 mEq/l) significantly increased after the infusion therapy (6.0 ± 1.7 mEq/l, p º 0.001). Repeat angiography showed vasodilatory effect on the spastic cerebral arteries at 3 hours after the infusion, especially in the arteries near to the site of cisternal drainage placement. The magnesium infusion also caused decreased mean arterial blood velocity in the spastic arteries in 6 of the 7 measured patients (162 ± 38 cm/sec to 114 ± 42 cm/sec, p º 0.001). Finally, 5 of the 10 patients achieved good recovery, 1 patient had moderate disability, 1 patient became severely disabled due to meningitis, and 3 patients were vegetative or dead, due to failure of magnesium irrigation in 1 patient and advanced age in the other 2 (more than 80 years old). This preliminary study indicates that intra-cisternal infusion of magnesium sulfate solution has vasodilatory effect on the spastic cerebral arteries after aneurysmal SAH.

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Section: Introductionmentioning

confidence: 99%

Initial Clinical Experience of Vasodilatory Effect of Intra-cisternal Infusion of Magnesium Sulfate for the Treatment of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Mori

Yamamoto

Nakao

et al. 2009

Neurol. Med. Chir.(Tokyo)

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“…Magnesium-induced favorable vascular effects have been demonstrated in many organ systems and previously discussed [12,13,26]. Therefore, these could explain how magnesium may have potential therapeutic effect in some diseases associated with perfusion abnormality via local microcirculatory disturbances and decreased blood flow such as NTG.…”

Section: Putative Therapeutic Effect In Glaucomamentioning

confidence: 95%

“…Magnesium may prevent glutamate induced neurotoxicity by blocking NMDA receptor related calcium influx and by inhibiting the release of glutamate, hence magnesium protect the cell against oxidative stress and apoptosis [23][24][25]. Indeed, other potential neuroprotective mechanism attributed for magnesium is considered to be increasing blood flow dependent of vasodilator effect on calcium channel blockade [15,26,27].…”

Section: Introductionmentioning

confidence: 99%

Magnesium: Effect on ocular health as a calcium channel antagonist

Korkmaz

Ekici²,

Tufan³

et al. 2013

J Clin Exp Invest

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ÖZETMagnezyum hücre zar fonksiyonlarını, düz kas kontraksiyonlarını ve enzimatik reaksiyonları etkileyerek pek çok metabolik sürece katılan fizyolojik bir kalsiyum kanal blokörüdür. Magnezyumun Endothelin-1 (ET-1) ve Nitrik Oksit (NO) yolakları vasıtasıyla endotel fonksiyonları-nı modifiye ederek dokulara kan akımında artışa neden olduğu gösterilmiştir. Magnezyum aynı zamanda N-metil-D-aspartat (NMDA) reseptör ilişkili kalsiyum içe akımı-nı bloke ederek ve glutamat serbestleşmesini önleyerek nöroprotektif rol oynamakta ve hücreleri oksidatif stres ve apoptoza karşı korumaktadır. Hem kan akımında artışa neden olması hem de nöroprotektif etkileri magnezyumu glokom çalışmaları için iyi bir hedef molekül yapmaktadır. Magnezyumun retinada oksidatif stresi ve apoptozu azalttığı ve ganglion koruyucu etkileri olduğu gösterilmiştir. Bir takım çalışmalarda aynı zamanda magnezyumun diabetik hastalarda insulin resistansını azalttığı, glisemik kontrolü kolaylaştırdığı ve retinopatiyi önlediği gösterilmiştir. Magnezyumun lensteki iyon dengesinin sağlanmasında kritik önemi belirlenmiştir. Magnezyum eksikliğinin lentiküler oksidatif stresi arttırdığı ve iyon dengesini bozarak katarakt oluşumuna neden olduğu gösterilmiştir.Anahtar kelimeler: Magnezyum, kalsiyum kanal blokajı, glokom, nöroproteksiyon, diabetik retinopati, katarakt ABSTRACTMagnesium is the physiologic calcium channel blocker, involving in many different metabolic processes by maintaining cell membrane function, modulating smooth muscle contraction and influencing enzymatic activities. Magnesium has been shown to increase blood flow to tissues by modifying endothelial function via endothelin-1 (ET-1) and nitric Oxide (NO) pathways. Magnesium also exhibits neuroprotective role by blocking N-methyl-D-aspartate (NMDA) receptor related calcium influx and by inhibiting the release of glutamate, hence protects the cell against oxidative stress and apoptosis. Both increase in blood flow and its neuroprotective effect make magnesium a good candidate for glaucoma studies. Magnesium has been shown to decrease oxidative stress and apoptosis in retinal tissue and to have retinal ganglion cell sparing effect. A series of studies has been conducted about magnesium could decrease insulin resistance in diabetic patients, ease glycemia control and prevent diabetic retinopathy. Magnesium is found to be critically important in maintaining normal ionic homeostasis of lens. Magnesium deficiency has been shown to cause increased lenticular oxidative stress and ionic imbalance in the lens so trigger cataractogenesis. J Clin Exp Invest 2013; 4 (2): 244-251

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“…A series of clinical trials has been launched to assess the ability to reduce secondary neurological deficits after SAH. Several small observational studies and placebocontrolled studies using different doses of intravenous magnesium sulfate produced promising results [56][57][58][59][60][61]. In a randomized, placebocontrolled multicenter study conducted by van den Bergh et al, patients received a daily dose of 64 mmol MgSO 4 for 14 days.…”

Section: Magnesium Sulfatementioning

confidence: 99%

Neuroprotective Treatment Strategies for Delayed Cerebral Ischemia after Subarachnoid Hemorrhage – Review of Literature and Future Prospects

Westermaier¹

2013

J Neurol Neurophysiol

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Magnesium sulfate therapy after aneurysmal subarachnoid hemorrhage

Cited by 185 publications

References 17 publications

Initial Clinical Experience of Vasodilatory Effect of Intra-cisternal Infusion of Magnesium Sulfate for the Treatment of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Initial Clinical Experience of Vasodilatory Effect of Intra-cisternal Infusion of Magnesium Sulfate for the Treatment of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Magnesium: Effect on ocular health as a calcium channel antagonist

Neuroprotective Treatment Strategies for Delayed Cerebral Ischemia after Subarachnoid Hemorrhage – Review of Literature and Future Prospects

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