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Can Magnesium Sulphate Prevent Cerebral Ischemic Injury? An Experimental Study and Neuroradiological Evidence Cem Atabey, Soner Şahin, Serdar Kahraman, Nail Bulakbaşı

Yazar: Materyal türü: MakaleMakaleDil: İngilizce Yayın ayrıntıları:2015.ISSN:
  • 1300-1817
Konu(lar): LOC sınıflandırması:
  • WL355
İçindekiler: Journal of Neurological Sciences 2013, Vol. 30 Issue 1, p30-39. 10p. Özet: This study was designed to investigate whether magnesium sulphate prevents cerebral ischemic injury on an experimental rat model. Forty Sprague-Dawley rats were divided into 4 groups: I) the sham group; II) the group to which saline was applied prior to ischemia (control); III) the group that received MgSO4 (90 mg/ kg) intraperitoneally 30 minutes before ischemia; IV) the group that received MgSO4 (90 mg/ kg) intraperitoneally 30 minutes after ischemia. Infarct volumes were measured in all the rat groups by the use of MRI subsequently analyzed by the Workstation: Philips Easy Vision 5.2.1.1 Measurement analysis program. Total infarct volumes in the ischemic group that received saline without MgSO4, in the group that received MgSO4 after occlusion of the MCA and in the group that received MgSO4 before MCA occlusion were 231.7±34.03 mm³, 158.85±32.16 mm³ and 87.35±22.27 mm³ respectively. Total infarct volumes were significantly reduced in both the pre-occlusive and post-occlusive MgSO4 treatment groups (p<0.001). Our results support that magnesium displays a neuroprotective impact against cerebral ischemic injury. This therapeutic potential may have important clinical applicability if applied before neurovascular surgical interventions. However, the actual therapeutic potential of magnesium in humans and standardization of protocols need to be unveiled in further studies.
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Online Electronic Document NEU Grand Library Online electronic WL355 .C36 2013 (Rafa gözat(Aşağıda açılır)) Ödünç verilmez EOL-862

This study was designed to investigate whether magnesium sulphate prevents cerebral ischemic injury on an experimental rat model. Forty Sprague-Dawley rats were divided into 4 groups: I) the sham group; II) the group to which saline was applied prior to ischemia (control); III) the group that received MgSO4 (90 mg/ kg) intraperitoneally 30 minutes before ischemia; IV) the group that received MgSO4 (90 mg/ kg) intraperitoneally 30 minutes after ischemia. Infarct volumes were measured in all the rat groups by the use of MRI subsequently analyzed by the Workstation: Philips Easy Vision 5.2.1.1 Measurement analysis program. Total infarct volumes in the ischemic group that received saline without MgSO4, in the group that received MgSO4 after occlusion of the MCA and in the group that received MgSO4 before MCA occlusion were 231.7±34.03 mm³, 158.85±32.16 mm³ and 87.35±22.27 mm³ respectively. Total infarct volumes were significantly reduced in both the pre-occlusive and post-occlusive MgSO4 treatment groups (p<0.001). Our results support that magnesium displays a neuroprotective impact against cerebral ischemic injury. This therapeutic potential may have important clinical applicability if applied before neurovascular surgical interventions. However, the actual therapeutic potential of magnesium in humans and standardization of protocols need to be unveiled in further studies.

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