Pulmonary Response to Hyperoxia: Effects of Magnesium

Abstract

Animals and humans rapidly develop respiratory failure and die within a few days when exposed to 100% oxygen. Postmortem examination of the lungs shows histopathologic features characteristic of diffuse alveolar damage, clinically recognized as adult respiratory distress syndrome (ARDS). At the present time, there is no effective therapy available to alter outcomes in ARDS. Importantly, hypomagnesemia also is frequently observed in critically ill patients at risk of developing ARDS. In a model of hyperoxic lung injury, rats were exposed to 100% oxygen for 48, 64, and 96 hr and several experiments were performed. First, changes in the features of bronchoalveolar lavage and in alveolar macrophage function were compared in rats exposed to room air and those exposed to hyperoxia. Second, we studied the effect of hypomagnesemia on the severity of hyperoxic lung injury. Third, we evaluated the pulmonary responses to high-dose and normal-dose Mg therapy in rats exposed to hyperoxia. In all groups, hyperoxia induced significant changes in the total and differential cell counts with increased lipid peroxidation of lavaged cells, enhanced chemiluminescence from alveolar macrophages, and protein leakage into the alveolar spaces. After 48 hr of hyperoxia, oxygen-free radical formation and hydrogen peroxide production by the alveolar macrophage were diminished compared to baseline, implying a toxic effect of hyperoxia on the alveolar macrophages. Overall, hypomagnesemia tended to magnify the degree of hyperoxic lung injury, while high-dose Mg therapy tended to attenuate the effects of hyperoxia. In conclusion, in this animal model of diffuse alveolar damage, alterations in host serum magnesium levels may modulate the degree of lung damage. -Environ Health Perspect 102(Suppl 10): 101-105 (1994)

Prevention of Hyperoxia‐Induced Alterations in Synaptosomal Membrane‐Associated Proteins by N‐tert‐Butyl‐α‐Phenylnitrone and 4‐Hydroxy‐2,2,6,6‐Tetramethylpiperidin‐1‐oxyl (Tempol)

“…There is evidence that hy~eroxiamay be related to chronic lung disease in premature infants (Kelly, 1993). Another group found that in both animals and humans, exposure to 100% oxygen causes adult respiratory distress syndrome from which death results within a few days (Dedhia and Banks, 1994). Prolonged exposure to high concentrations of oxygen is reported to cause CNS and pulmonary toxicity, resulting in atelectasis, pulmonary edema, and seizures (Jenkinson, 1993).…”

Magnesium Is a Vital Ion in the Body—It Is Time to Consider Its Supplementation on a Routine Basis

“…Exposure to a high fraction of oxygen damages the respiratory epithelium and causes long-term fibrosis and mortality in animals and humans. In contrast, high-dose magnesium therapy has been found to alleviate the adverse effects of hyperoxia [ 52 ]. Hypomagnesemia has been found to be associated with a higher risk of mortality, sepsis, mechanical ventilation, and extended intensive care unit (ICU) stays for patients who are admitted to the ICU.…”

A Stress Repair Mechanism That Maintains Vertebrate Structure During Stress

“…Thrombin activity requires Ca + , and parathyroid glands regulate extracellular Ca + to optimize its activity [26,[66][67][68][69][70][71][72][73][74][75][76][77][78][79]. Mg + competitively inhibits Ca + and mitigates thrombin activity [66,75,[80][81][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96].…”