EFFECT OF L-ARGININE ON PROLIFERATION AND APOPTOSIS OF PULMONARY ARTERY SMOOTH MUSCLE CELLS AND ENDOTHELIAL CELLS IN PULMONARY HYPERTENSION SECONDARY TO A LEFT-TO-RIGHT SHUNT

Wei B, Du JB, Qi JG,

Department of Pediatrics, First Hospital, Peking University, Beijing, China

 

Objective: Currently, more and more investigations demonstrated that L-arginine, a precussor of nitric oxide, was a promising agent in the treatment of pulmonary hypertension. The present research was conducted to study the mechanisms by which it attenuated pulmonary hypertension secondary to left-to-right shunt by examining the effect of L-arginine on proliferation and apoptosis of pulmonary artery smooth muscle cells (SMC) and endothelial cells (EC) in pulmonary hypertension.

Methods: Pulmonary hypertension of rats was induced by aorta and inferior vena cava shunting procedure. Immunohistochemistry for PCNA and FAS expressions and TUNEL (TdT-mediated dUTP-biotin nick and labeling) were used to detect cell proliferation and apoptosis.

Results: Proliferative indexes (PI) of pulmonary artery SMC and EC in the shunting group elevated obviously compared with that of control group (p< 0.01), however, it was significantly reduced by L-arginine (p< 0.01). Apoptotic indexes (AI) of pulmonary artery SMC and EC in the shunted rats also elevated compared with that of control group (p< 0.05), but it was augmented in shunting +L-arginine rats (p< 0.01). Meanwhile, the expressing integral score of Fas in shunting group elevated (p< 0.01), and it was again augmented by L-arginine (p<0.01).

Conclusion: L-arginine could inhibit proliferation and promote apoptosis of pulmonary artery SMC and EC in shunted rats, which might provide theoretical basis for the therapy of the pulmonary hypertension secondary to left-to-right shunt.

 
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