Résumé
Objective: To establish an in vitro vascular model to study the impact of different blood oxygen (O2) saturation on main pulmonary artery pressure changes in order to further explore the mechanism of pulmonary hypertension. Methods: 20 New Zealand white rabbits were randomly divided into 4 groups: Normal control group and 3 experimental groups as High O2 (90%-100%)saturation group, Middle O2 (65%-75%)saturation group and Low O2 (40%-50%) saturation group, n=5 in each group. The in vitro pulmonary artery segments were treated with fresh heparinized rabbit blood and connected to extracorporeal circulation system for 48h at perfusion pressure at 40 mmHg; the condition of O2 saturation was regulated by membrane oxygenator. Pathological morphology was compared among different groups. Results:The bypass time in all 3 groups was 48h and the pressure was stably controlled at 40 mmHg. Blood O2 contents in High O2 saturation group, Middle O2 saturation group and Low O2 saturation group were (97.94±1.01) %, (72.14±12.85) %and (43.83±8.71) % respectively, P<0.05. Pathological analysis indicated that compared with Normal control group, 3 experimental groups had increased thickness in pulmonary artery wall; upon O2 saturation decreasing, the elastic fibers in pulmonary artery became increasing and more thickening accordingly. Conclusion: We established an in vitro vascular model to study the impact of different blood O2 saturation on main pulmonary artery pressure changes in experimental rabbits.
Résumé
Objective: To establish an in vitro vascular model to study the impact of different blood oxygen (O2) saturation on main pulmonary artery pressure changes in order to further explore the mechanism of pulmonary hypertension. Methods: 20 New Zealand white rabbits were randomly divided into 4 groups: Normal control group and 3 experimental groups as High O2 (90%-100%)saturation group, Middle O2 (65%-75%)saturation group and Low O2 (40%-50%) saturation group, n=5 in each group. The in vitro pulmonary artery segments were treated with fresh heparinized rabbit blood and connected to extracorporeal circulation system for 48h at perfusion pressure at 40 mmHg; the condition of O2 saturation was regulated by membrane oxygenator. Pathological morphology was compared among different groups. Results:The bypass time in all 3 groups was 48h and the pressure was stably controlled at 40 mmHg. Blood O2 contents in High O2 saturation group, Middle O2 saturation group and Low O2 saturation group were (97.94±1.01) %, (72.14±12.85) %and (43.83±8.71) % respectively, P<0.05. Pathological analysis indicated that compared with Normal control group, 3 experimental groups had increased thickness in pulmonary artery wall; upon O2 saturation decreasing, the elastic fibers in pulmonary artery became increasing and more thickening accordingly. Conclusion: We established an in vitro vascular model to study the impact of different blood O2 saturation on main pulmonary artery pressure changes in experimental rabbits.