Changes And Significance Of CF6,6-keto-PGF_1α In Plasma Following Acute Pulmonary Embolismin In Rabbit

Objective: The pulmonary embolism is an clinic syndrome caused by endogenous or exogenous embolus obstruct pulmonary artery. When APE happens, Increasing of pulmonary vascular resistance and pulmonary artery pressure is pathophysiological base in APE. Embolic effection of"mechanical obstruction"is immediate cause about increasing of pulmonary vascular resistance. In addition, Neurohumor has also possessed important effection on change of pulmonary circulation in embolism earliar period. Study shows 6-ketoprostaglandin F1α(6-keto-PGF1α) is related to pulmonary artery hypertension. Besides, chondrosome coupling factors 6 (CF6) is a unique endogenous inhibitor of 6-keto-PGF1α. The two kinds of vasoactive substance may produce an important influence on the pulmonary hemodynamic after APE. So we set up APE model and detection the changes of CF6 and 6-keto-PGF1αin plasma, and relation between the two kinds and pulmonary artery hypertension. In order to investigate their effects on hemodynamics and the possible mechanisms of pulmonary artery hypertension following APE.Method:sixty-four New Zealand rabbits, weighing 2.5～ 3.5kg,the male and female were given consideration to, were obstructed the left lower lung artery by inflating gas of 5F Berman sacculus catheter to set up rabbit APE model.The animals were randomly divided into eight groups:(1) control group(n=8), (2)sham operation group(n=8), (3)embolism 1h group(n=8), (4)embolism 2h group(n=8), (5)embolism 4h group(n=8), (6)embolism 8h group(n=8) (7)embolism 12h group(n=8) (8)embolism 24h group(n=8). We monitored the pulmonary arterial mean pressure (PAMP) at pre-embolization, embolization instantly, embolization1h, 2h, 4h, 8h, 12h and 24h. We detected the content of CF6 and 6-keto-PGF1αin plasma by ratio-immunity method, and calculate CF6/6-keto- PGF1αratio at pre-embolization, embolization instantly, emboli- zation 1h, 2h, 4h, 8h, 12h and 24h. We monitored the relationship between the two and pulmonary artey hypertensionResults:(1)The channes of lung hemodynamics before and after embolism :PAMP was rapidly increased after embolis, and was obvously higher than pre-embolization and sham group lever (P<0.05, respectively). PAMP was decreased gradually at embolization 0.5h,1h,but still higher significantly than pre- embolization(P<0.05,respectively). PAMP was decreased to the pre-emblization and sham group level at embolism 2h 4h and 8h. PAMP was increased again at embolism 12h and 24h, and was higher than pre-embolization and sham group lever (P<0.05, respectively) (2)The changes of CF6 in plasma: except for the control group, the sham operation group and embo1ism instantly, (141.64±14.87,141.55±12.60,140.88±9.30 P>0.05 respectively) the content of plasma CF6 were higher significantly at embolization lh, 2h, 4h, 8h, 12h and 24h than pre-embolization(183.52±9.80,188.73±7.32,188.74±9.67, 189.76±7.78, 228.02±9.63, 238.62±5.65, P<0.05 respectively) the content of plasma CF6 were higher at embolization 8,12h and 24h than embolization 1h, 2h and 4h. (189.76±7.78, 228.02±9.63, 238.62±5.65, P<0.05, respectively)and gradually increased accompanied the prolongation of embolization.When contrasting to the value of corresponding time in different groups, the content of embolization 24h were higher than embolization 12h group (238.62±5.65 P<0.05 , respectively) . (3)The change of 6-keto-PGF1αin plasma: The content of plasma 6-keto-PGF1αwere higher significantly at embolization 1h, 2h, 4h, 8h, 12h and 24h than pre-embolization and the sham operation group (203.81±8.99, 121.08±7.63, 123.06±8.43, 123.13±7.21, 125.35±6.82, 126.48±4.29, P<0.05 , respectively) . At embolization 1h, the content of plasma 6-keto-PGF1αachieved peak(139.50±10.20, P<0.05,respectively). The content of plasma 6-keto-PGF1αgradually decreased at embolismation 2h, 4h, 8h, 12h and 24h. there was not significant difference at embolismation 4h, 8h, 12h and 24h(123.06±8.43, 123.13±7.21, 125.35±6.82, 126.48±4.29 P>0.05, respectively). (4)The changes of CF6/6-keto-PGF1αratio: CF6/6-keto-PGF1α(C/P) ratio were not significant difference at control group, sham group and embolization 2h, 4h and 8h. (1.45±0.15, 1.44±0.11, 1.57±0.09, 1.57±0.11, 1.58±0.02 P>0.05, respectively). C/P ratio decreased to reach perigee at embolization 1h , were lower than embolization every time point (0.97±0.06 P<0.05, respectively). T/P ratio at emboliza- tion 12h and 24h were higher than pre-embolization and sham group lever (1.87±0.09, 1.92±0.02 P<0.05, respectively).Conclusion:(1)The experimental animal model of APE owns the advantages in convenient controllability and easy reproduci- bility.(2)CF6 and 6-keto-PGF1αparticipate pulmona- ry vascular reaction, hemodynamic changes, pulmonary artery hypertension. (3)CF6 as a factor can montior formation of pulmonary hypertension and blood vessel endothelium injury.