动物造模,西藏小型猪缺氧缺血性脑病模型 z-bo 2021-01-08 347

　　Objective: To establish a hypoxic-ischemic encephalopathy model in Tibetan mini-pigs, observe the MR manifestations of the HIE model, and compare with the pathological results.

　　Method: 6 1 to 3 days old Tibetan miniature pigs (4 in the model group and 2 in the control group). In the model group, the common carotid arteries on both sides were clamped and placed in a hypoxic box (oxygen concentration 8%). After 60 minutes, reoxygenation and reperfusion were performed. In the control group, only the common carotid arteries on both sides were separated. In the model group, brain ESWAN tests were performed at 2, 24 hours, 3 days and 5 days after the model was established. The control group received enhanced brain T2*weighted angiography (enhanced T2 star weighted angiography, ESWAN) 2 hours after surgery. Within 24 hours after the model was established, the SE sequence T2FLAIR, T2WI and DWI were used for routine MR examination. Finally, perform a pathological examination.

　　Result: The T 2 * value of the new striatum reached a peak 3 days after the model was established, and there was a statistically significant difference between the T 2 * value of the control group (P) at each point. (U003c0.05). 24 hours after the model was established, the T2* value of the white area under the cortex reached its peak (P\u003c0.05). After the model was established, the R2* value of the new striatum reached at least 3 days, and the difference from the control group at different time points was statistically significant (P\u003c0.05). 24 hours after the model was established, the R2* value of the white area under the cortex reached the lowest value (P\u003c0.05). After the model was established, the amplitude value increased significantly (P\u003c0.05). In the DWI imaging of the MR brain of the animal in the model group, the signals of the bilateral subfrontal white matter and the bilateral neostriatum were slightly higher, the T2FLAIR signal changes were not obvious, and there was no obvious abnormality on T2WI, I proved. SWI showed macroscopic spinal veins and microbleeds. The early pathological changes of HIE are mainly edema and venous congestion, sometimes accompanied by local necrosis and hemosiderin deposition.

　　 Conclusion: ESWAN sequence can assess whether HIE has hemorrhage and brain tissue edema. T2 *, R2 * and amplitude values can be used to observe the onset and changes of hypoxic-ischemic brain injury.