ObjectiveTo compare the injury to hepatocarcinoma and normal liver tissues following ischemia and reperfusion. MethodsThe hepatocarcinoma(HC) models were established by injectin of VX2 tumor (tissue) suspension fluid into the left-middle lobe of liver of rabbits. After the models were established, the models left hepatic vessels were occluded for 60 minus, then followed by various intervals of reperfusion, and the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured, and apoptotic (changes) in the hepatocarcinoma and normal hepatic tissues were observed by means of HE staining and TUNEL method. ResultsThe concentration of SOD decreased significantly in hepatocarcinoma tissue and reached the lowest point at 1h after ischemia and reperfusion (64.594.97NU/mgprot), then gradually rebounded, but, at 7d after reperfusion, it still retained at a lower level(121.126.88NU/mgprot) than that before reperfusion. In contrast with normal liver tissues,the concentration of MDA decreased in the hepatocarcinoma tissues following ischemia and reperfusion, the changs of MDA were similar to SOD. The apoptotic cells in hepatocarcinoma tissues increased to the highest point at 1 day following reperfusion, but 7d after reperfusion, the number of positive cells were more than before reperfusion, and the apoptotic rate was higher in (hepatocarcinoma) tissues compared with the normal liver tissues. ConclusionsIn comparison with normal liver tissue, hepatocarcinoma tissue is more suscepible to the injury of ischemia and reperfusion.

Objective To explore the characteristics of the flow velocity waveform of superior vena cana (SVC) in a rat model with chronic monocrotaline-induced pulmonary hypertension by echocardiography.Methods The chronic pulmonary hypertension model was developed by monocrotaline solution (60 mg/kg) injection into the abdominal cavity in 32 SD rats.Eight rats with the placebo injected served as controls.An examination of the flow velocity waveform of SVC was performed by Doppler echocardiography via supraclavicular fossa before and 28-day after the injection.The pulmonary arterial systolic pressure was measured by pressure-guided micro-catheter 28-day after the injection both in the control and the pulmonary hypertension model group.Results Chronic monocrotaline-induced pulmonary hypertension was successfully developed in 29 rats.The flow velocity waveform of SVC showed that the ratio of the maximum reverse peak flow velocity due to atrial contraction (VAR) to the maximum systolic peak flow velocity (Vs) and VAR increased dramatically 28-day after the monocrotaline solution injection in both sides of SVC (P ＜0.01), while only the Vs of the right SVC significantly decreased (P ＜0.05).Conclusions The changes of VAR/Vs ratio and VAR in rat model with chronic monocrotaline-induced pulmonary hypertension suggested that the changes of flow velocity waveform of SVC have indicating features in reflecting pulmonary hypertension.

Objective To establish a canine model with acute thrombo-embolic pulmonary hypertension monitored by echocardiography. Methods Simulated the pathophysiologic process of acute thrombo-embolic pulmonary hypertension in human, the canine model was developed. The femoral vein puncture and the right heart catheterization to monitor pulmonary artery pressure were operated guided by echocardiography, while the autologous blood clot was injected to the contralateral femoral vein. The criteria of model was the pulmonary artery systolic pressure was higher than 30 mmHg. Results Echocardiography can accurately guide the placement of right heart catheterization and ancillarily observe the pressure testing of pulmonary artery. Of twenty seven healthy experiment dogs, twenty four models with acute thromboembolic pulmonary hypertension were successfully developed. The successful rate was 88.9 %. Conclusions This canine model with acute thrombo-embolic pulmonary hypertension guided by echocardiography is easy to operate and its repeatability is good.