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Pulmonary vascular dilation induced by l‐arginine: correlation with induction of endothelial nitric oxide synthase in a rabbit model

Purpose: To determine whether oral administration of l‐arginine induces pulmonary vascular dilation, and if this pulmonary vascular dilation correlates with induction of endothelial nitric oxide synthase (eNOS) in a rabbit model. Material and Methods: Seven rabbits were fed with l‐arginine dissolved in tap water. The degree of pulmonary vascular dilation was determined using thin‐section computed tomography and the concentration of serum nitrite was measured. They were compared with four control animals. The pulmonary vascular dilation was correlated to serum levels of nitrite. Lung tissues were examined for induction of eNOS by immunohistochemistry. Results: An increased degree of pulmonary vascular dilation was found in the l‐arginine‐fed group compared to the control group (P<0.05). Serum levels of nitrite in the l‐arginine‐fed group were higher than those in the control group (P<0.05). Pulmonary vascular dilation correlated with serum levels of nitrite (r2  = 0.95, P<0.05). Induction of eNOS was increased in the l‐arginine‐fed group. Conclusion: The administration of l‐arginine causes pulmonary vascular dilation, which is most likely mediated via nitric oxide through increased induction of eNOS in a rabbit model.