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.