摘要： Abstract: Objective To determine the role of asymmetric dimethylarginine (ADMA) in acute lung injury induced by cerebral
ischemia/reperfusion (I/R) injury in rats. Methods Adult male SD rats were randomly divided into 4 groups, namely the
sham-operated group (S), cerebral I/R model group, ADMA + I/R group, and dimethylarginine dimethylaminohydrolase
(DDAH)+I/R group. In the latter 3 groups, acute lung injury was induced by left middle cerebral artery occlusion for 120 min.
After a 24-h reperfusion, the rats were sacrificed and the activities of nitric oxide synthase (NOS) and contents of nitric oxide
(NO) were measured using reductase and colorimetric assay. The mRNA and protein expressions of protein kinase C (PKC)
and myosin light chain kinase (MLCK) in the lung tissues were detected with RT-PCR and Western blotting, respectively. The
contents of ADMA in the bronchoalveolar lavage fluid (BALF) and blood flowing into and out of the lungs were measured by
ELISA. Results Cerebral I/R injury caused significantly elevated ADMA levels in the BALF and blood flowing into the lungs,
and obviously lowered the NO concentration and NOS activity in the lung tissues (P<0.05). Following cerebral I/R injury,
MLCK and PKC mRNA and protein expressions were significantly upregualted in the lung tissues (P<0.05). Exogenous DDAH
obviously decreased the levels of ADMA in the BALF and blood flowing into the lungs, increased NO concentration and NOS
activity, and down-regualted MLCK and PKC mRNA and protein expressions in lung tissues of rats with cerebral I/R injury
(P<0.05). Conclusion ADMA contributes to the development of acute lung injury following cerebral I/R injury in rats by
upregulating MLCK and PKC expression. ADMA may serve as a novel therapeutic biomarker and a potential therapeutic target
for acute lung injury induced by cerebral I/R injury.