Effect of beta-adrenergic agonist on alveolar fluid clearance in rats with acute lung injury

Background

Although it is well known that beta-adrenergic agonist improves alveolar fluid clearance (AFC) in several animal species, it is not known whether beta-adrenergic agonist improves AFC in infectious acute lung injury (ALI). This study is aimed at investigating the effect of beta-adrenergic agonist (dobutamine) on AFC in rats with infectious ALI and exploring the associated mechanism.

Methods

Thirty-two male Sprague–Dawley rats were randomly divided into four groups (normal control group, ALI group, dobutamine control group, dobutamine treatment group). A rat with ALI was induced by infusion of endotoxin intravenously. Alveolar fluid clearance was measured by the single-nuclide tracer technique. α-Rat epithelial sodium channel (α-rENaC), β-rENaC and γ-rENaC mRNA expressions were measured by RT-PCR.

Results

AFC of the ALI group was 14.0 ± 1.2%, which was significantly lower than the normal control group (21.0 ± 3.9%), the dobutamine treatment group (20.0 ± 3.8%) and the dobutamine control group (26.6 ± 1.6%) (P < 0.05). AFC of the dobutamine control group was significantly higher than the normal control group, dobutamine treatment group and ALI group (P < 0.05). α-rENaC and β-rENaC mRNA expressions of the ALI group (1.4 ± 0.4 and 0.7 ± 0.8, respectively) and the dobutamine treatment group (1.38 ± 0.13 and 0.71 ± 0.17, respectively) were significantly higher than the dobutamine control group (1.01 ± 0.14 and 0.58 ± 0.12, respectively) and the normal control group (1.00 ± 0.28 and 0.44 ± 0.11, respectively) (P < 0.05). There were no significant differences of α-rENaC and β-rENaC mRNA expressions between the normal control group and dobutamine control group, and no significant difference between the ALI group and dobutamine treatment group (P > 0.05). γ-rENaC mRNA expressions of the dobutamine control group and dobutamine treatment group were 0.90 ± 0.19 and 0.97 ± 0.15, respectively, which were significantly higher than normal control group (0.69 ± 0.10) and the ALI group (0.7 ± 0.3) (P < 0.05). There was no significant difference of γ-rENaC mRNA expressions between the normal control group and the ALI group, and no significant difference between the dobutamine control group and the dobutamine treatment group (P > 0.05).

Conclusion

Beta-adrenergic agonist may upregulate γ-rENaC expression and improve AFC in rats with endotoxin-induced ALI. It may be beneficial to increase AFC and reduce lung edema using beta-adrenergic agonist in ALI patients.