Rationale: The mechanical ventilation may aggravate the severe acute lung injury and trigger a systemic inflammatory response. The pathophysiology evolves Biotrauma, meaning that the over distension and the cyclical opening/collapse of structures on the lung during ventilation with high PIP associated with low PEEP, results in excessive activation of nuclear factor-{kappa}Beta (NF-κB), a regulator of the inflammatory response, that exacerbates the local response and becomes it systemic. The magnesium, a modulator of signaling pathways of the inflammatory cascade, deserves investigation in inhibiting the NF-κB activation.
Objectives: Investigate experimentally the effect of hypermagnesemia to inhibit the activation and migration of NF-κB from cytoplasm to nucleus in cells of lungs injured by mechanical ventilation.
Methods: Two experimental groups of 15 Sprague-Dawley rats each, one receiving 1.25 mL/kg/h of a 10% MgSO4 solution, other receiving equal volume of saline, both under mechanical ventilation with VT of 40 mL/kg, PEEP of 3 cmH2O, PIP of 35 cm H2O, RR of 40 cycles per minute. Lungs were excised after 50 minutes of experimental interventions and prepared for further immunohistochemical analysis.
Measurements and Main Results: ANOVA shown no differences when compared the NF-κB activation values in the cytoplasm (712.44 ± 253.86) and nucleus (974.27 ± 344.59) of cells in MgSO4 group with the respective values in cytoplasm (653.99 ± 272.98) and nucleus (952.29 ± 346.68) of cells in Saline group (F[1, 28] = 0.90, p > .05).
Conclusions: There was no inhibitory effect of magnesium on the activation of NF-kB nor on its expression through migration to the nucleus.