TY - JOUR
T1 - Enhanced expression of nitric oxide synthase in the early stage after increased pulmonary blood flow in rats
AU - Chou, Tsai Fwu
AU - Wu, Ming Shiou
AU - Chien, Chiang Ting
AU - Yu, Chia Cherng
AU - Chen, Chau Fong
N1 - Funding Information:
This work was supported by the Cardiac Children’s Foundation of the Republic of China. The authors thank Ms Yu-Chen Su for her excellent technical assistance in performing the experiments.
PY - 2002
Y1 - 2002
N2 - Objective: Evidence that vasodilator nitric oxide mediates normal pulmonary vascular tone has led to the hypothesis that endothelial injury induced by congenital heart disease with increased pulmonary blood flow disrupts these regulatory mechanisms and its associated altered vascular reactivity. Therefore, we hypothesized that increased pulmonary blood flow results in altered expression of endothelial nitric oxide synthase (eNOS). Methods: We created an arteriovenous shunt in female Wistar (5-week-old) and measured the change of pulmonary blood flow and pressure immediately after and 1 month after the shunt operation. The protein levels of eNOS in the lung tissues of rats were assessed. Results: The shunt immediately resulted in a significant increase in pulmonary blood flow (16.5±2.7%), pulmonary artery pressure (2.3±0.7mmHg), and blood O2 saturation (16.1±11.8%) in the pulmonary artery. After 4 weeks, there was a significant increase in pulmonary blood flow (30.7±1.6%), pulmonary artery pressures (4.3±1.1mmHg), and blood O2 content (43.3±17.5%). Western blot analysis demonstrated that eNOS protein was increased in the shunt lung 72h after surgery and recovered to the control level 1 week later. Conclusion: This simple shunt model can induce early upregulation of eNOS expression with increased pulmonary blood flow and pulmonary artery pressure in rats.
AB - Objective: Evidence that vasodilator nitric oxide mediates normal pulmonary vascular tone has led to the hypothesis that endothelial injury induced by congenital heart disease with increased pulmonary blood flow disrupts these regulatory mechanisms and its associated altered vascular reactivity. Therefore, we hypothesized that increased pulmonary blood flow results in altered expression of endothelial nitric oxide synthase (eNOS). Methods: We created an arteriovenous shunt in female Wistar (5-week-old) and measured the change of pulmonary blood flow and pressure immediately after and 1 month after the shunt operation. The protein levels of eNOS in the lung tissues of rats were assessed. Results: The shunt immediately resulted in a significant increase in pulmonary blood flow (16.5±2.7%), pulmonary artery pressure (2.3±0.7mmHg), and blood O2 saturation (16.1±11.8%) in the pulmonary artery. After 4 weeks, there was a significant increase in pulmonary blood flow (30.7±1.6%), pulmonary artery pressures (4.3±1.1mmHg), and blood O2 content (43.3±17.5%). Western blot analysis demonstrated that eNOS protein was increased in the shunt lung 72h after surgery and recovered to the control level 1 week later. Conclusion: This simple shunt model can induce early upregulation of eNOS expression with increased pulmonary blood flow and pulmonary artery pressure in rats.
KW - Arteriovenous shunt
KW - Nitric oxide synthase
KW - Pulmonary hypertension
KW - Shearing stress
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U2 - 10.1016/S1010-7940(01)01129-0
DO - 10.1016/S1010-7940(01)01129-0
M3 - Article
C2 - 11825745
AN - SCOPUS:0036167386
SN - 1010-7940
VL - 21
SP - 331
EP - 336
JO - European Journal of Cardio-thoracic Surgery
JF - European Journal of Cardio-thoracic Surgery
IS - 2
ER -