Study On Hemodynamics And HGF In Experimental Pulmonary Thromboembolism In Sheep

ObjectiveTo establish a sheep model of pulmonary thromboembolism(PTE) and to study the changes of PTE and urokinase(UK) thrombbolytic therapy on hemodynamics, arterial blood gas and the level of plasma hepatocyte growth factor(HGF).MethodsEighteen sheeps were divided into a control(C) group, a PTE model group, an UK thrombbolytic therapy group, with 6 sheeps each. The PTE model was established by interventional catheter infusion of autologous blood clots. Sheeps were treated with urokinase in UK group after the PTE models had been established. Sheeps in C group underwent the same anesthesia and operation except embolization. Monitor and record the pulmonary arterial systolic pressure(PAP), average arterial pressure, respiratory rate, heart rate, PaO₂, P_A-a DO₂, PaCO₂, detect the level of the plasma HGF by enzyme linked immunosorbent assay (ELISA) at different time points(before, immediately after and 0.5h, 1h, 2h, 4h, 6h, 8h after embolization). After experiment, chest was opened and lung tissue was obtained for microscopic examination. The data was analyzed by using SPSS 11.5 statistical software.ResultsThe surface of lung was smooth and glossy in C group. Atelectasis, engorgement, and hemorrhagic focus were observed on the surface of lung in PTE model group, which were relieved obviously in UK group. Alveolar wall was integrated in C group, thickened and leukocyte infiltrated, micrangium engorged, hemorrhaged in PTE model group, the pathological changes above were relieved obviously in UK group, but leukocytic infiltration was serious yet.There were no significant changes in PAP at different time points in C group. In PTE model group PAP was increased and reached a peak level immediately after embolization, and then decreased to the baseline level(before embolization) at 8h after embolization. PAP was increased temporarily after UK therapy(1h after embolization), decreased to the baseline level at 5h after UK therapy(6h after embolization), but it was increased at 7h after UK therapy (8h after embolization).There were no significant changes in respiratory rate at different time points in C group. In PTE model group tachypnea occured immediately after embolization,respiratory rate was decreased to the baseline level at 2h after embolization, lh after embolization in UK group.There were no significant changes in heart rate at different time points in C group. In PTE model group heart rate was increased immediately after embolization, and remained at a high level for 2 hours, then stabilized at a level which was still higher than the baseline level. Heart rate was decreased to the baseline level at 2h after embolization, but increased again at 8h after embolization in UK group.There were no significant changes in average arterial pressure at different time points in C group. It was increased immediately after embolization and decreased to the baseline level at 0.5h after embolization in PTE model group. The same change in UK group.There were no significant changes in PaO₂ at different time points in C group. In PTE model group PaO₂ was decreased immediately after embolization, retumed to the baseline level at lh after embolization. PaO₂ was increased after UK therapy, but there was no difference compared with the baseline level.There were no significant changes in P_A-aDO₂ at different time points in C group. In PTE model group P_A-aDO₂ was increased immediately after embolization, it retumed to the baseline level at 4h after embolization,2h in UK group.There were no significant changes in PaCO₂ at different time points in three groups.the level of plasma HGF had no obvious changes at different time points in C group.In PTE model group it was kept on increasing trend at O.5h after embolization, and wasn't decreased at 8h after embolization. The tendency was same in UK group, and there was no difference between two groups in the level of plasma HGF at the same time point.There was no the relationship among the level of plasma HGF, PAP and PaO₂ It was stable for the PTE model which was established by interventional catheter infusion of autologous blood clots, and it was easy to be managed.There were some following changes in the early stage in the successful PTE model:pulmonary hypertension, unstable vital signs, PaO₂ decreasing, and engorgement,hemorrhage, and leukocytic infiltration in the lung tissue. UK therapy increased PAP temporally but ultimately promoted the drawdown, stabilized vital signs, and relieved the pathological changes, but the inflammatory reaction was remained.The level of plasma HGF was kept on increasing trend in 8 hours after PTE and UK therapy, which might be a protective reaction while blood vessel was injuried. There was no the relationship among the level of plasma HGF, PAP and PaO₂.