Background
Lower limb ischemia-reperfusion (I/R) elicits oxidative stress and causes inflammation
in lung tissues that may lead to lung injury. Magnesium sulfate (MgSO4) possesses potent anti-oxidation and anti-inflammation capacity. We sought to elucidate
whether MgSO4 could mitigate I/R-induced lung injury. As MgSO4 is an L-type calcium channel inhibitor, the role of the L-type calcium channels was
elucidated.
Materials and Methods
Adult male rats were allocated to receive I/R, I/R plus MgSO4 (10, 50, or 100 mg/kg), or I/R plus MgSO4 (100 mg/kg) plus the L-type calcium channels activator BAY-K8644 (20 μg/kg) (n = 12 in each group). Control groups were run simultaneously. I/R was induced by applying
rubber band tourniquets high around each thigh for 3 h followed by reperfusion for
3 h. After euthanization, degrees of lung injury, oxidative stress, and inflammation
were determined.
Results
Arterial blood gas and histologic assays, including histopathology, leukocyte infiltration
(polymorphonuclear leukocytes/alveoli ratio and myeloperoxidase activity), and lung
water content, confirmed that I/R caused significant lung injury. Significant increases
in inflammatory molecules (chemokine, cytokine, and prostaglandin E2 concentrations) and lipid peroxidation (malondialdehyde concentration) confirmed
that I/R caused significant inflammation and oxidative stress in rat lungs. MgSO4, at the dosages of 50 and 100 mg/kg but not 10 mg/kg, attenuated the oxidative stress,
inflammation, and lung injury induced by I/R. Moreover, BAY-K8644 reversed the protective
effects of MgSO4.
Conclusions
MgSO4 mitigates lung injury induced by bilateral lower limb I/R in rats. The mechanisms
may involve inhibiting the L-type calcium channels.
Key Words
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Article info
Publication history
Published online: April 13, 2011
Received:
January 13,
2011
Identification
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© 2011 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
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- A Healthy Dose of Heavy Metal: Magnesium and Acute Lung InjuryJournal of Surgical ResearchVol. 178Issue 2
- PreviewAcute lung injury (ALI) and its more serious manifestation, acute respiratory distress syndrome (ARDS), are all too common occurrences in intensive care units around the world that create a large debt to society both in the short term [1] and the long term [2]. These clinical syndromes claim thousands of lives each year and have been the object of many high profile studies in the past two decades. Unfortunately, despite extensive research efforts, we still have relatively little we can do to treat this condition.
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