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Objective To study the mechanism of brain death-induced heart damage by observing the change patterns of morphological damage to the heart and related inflammatory factors after brain death and provide the experimental basis for heart transplantation by brain-dead donor.Methods The 30 rabbits were equally divided into two groups by the random digital table method:sham-operation group and brain death group.The rabbit brain death model was established in the brain death group,and the sham-operation group was given slow intracranial pressure.The rest treatments in the two groups were the same.At 2nd,6th and 8th h after operation,blood pressure,heart rate and respiratory rate were recorded.The damage of heart tissues was observed by HE staining.The plasma concentrations of IL-1,IL-6 and IL-8 were tested by ELISA.The expression of some inflammatory factors in heart issues was detected by RT-PCR and immunohistochemistry.Results At 8 h after brain death,there was no signifiant difference in blood pressure and heart rate between two groups (P＞0.05).The damage of heart issues in the brain death group was more serious than in the shamoperation group.With the prolongation of brain death,the plasma concentrations of IL-6 and IL-8 increased significantly in the brain death group (P＜0.05),but the concentration of IL-1β showed no siginificant difference between the two groups at 2 h after brain death (P＜0.05).Besides,the expression of HSP27 and HSP70 mRNA as well as the protein expression of ICAM and NF-κB was significantly increased in the brain death group as compared with that in the sham-operation group (P＜0.05).Conclusion With the prolongation of brain death time,the inflammatory factors in the heart tissues and plasma interleukin were increased,suggesting the inflammatory reaction occurs in donor heart under the condition of brain death,which influences the quality of donor in the heart transplantation.
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[Objective]To observe the nerve regeneration and functional recovery in the adult rats.[Method]The sciatic nerves on the left side of 15 rats were exposed and 1.0 cm long segments of the nerves were removed from the mid-thigh level and replaced by rabbit nerve made acellular through chemical extraction.At 4 months after procedure,the nerve regeneration and function recovery were examined with HE staining,NF-160 immunohistochemical staining,electrophysiological tests and sciatic functional index(SFI).[Result]In the rats repaired by acellular nerves,regenerated axons re-entered into the acellular xeno-nerve segments without excessive sign of inflammation following implantation.As stimuling(1.5 mA,0.1 ms,1.0 Hz) to the proximal sciatic nerves,the implanted segment resulted in motor evoked potentials,which were recorded from posterior tibial muscles.SFI showed a partial recovery of locomotion of the limb with sciatic nerve defect.[Conclusion]Sciatic nerves defect can be repaired by chemical acellular xenogeneous nerves in rats.There was partial functional recovery,which revealed the grafting with chemical acellular xenogeneous nerves may be a promising mehod for nerve defect in clinical.
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Objective To observe the nerve regeneration and functional recov er y in canines, in which a large gap was made in the continuity of the sciatic ner ve and the gap was repaired by acellular allograft through chemical extraction. Methods 15 canines were divided into acellular nerve allografting group (ANG, 6 canines), autografting group (AG, 6 canines) and fresh nerve allografting group (FNG, 3 canines). The sciatic nerves on the right side of all animals were expos ed and 5.0 cm long segments were removed from the mid-thigh level and replaced by one of the three types of grafts. The motor recovery was assessed by gait tes t at month 6 postoperatively. The sensory and motor conducting functions were as sessed by electrophysiological experiments. The nerve regeneration was revealed by morphological studies on the grafting segments, the distal tibial nerves and motor end-plate of the target muscle. Results All the animals in ANG and AG gro ups had similar patterns of right posterior limb gait cycle and right ankle move ments. Stimuli (1.0-2.0 mA, 0.1 ms, 1.0 Hz) to the sciatic nerves proximal to t he implanted segment resulted in motor-evoked potentials recorded from the musc ulus triceps surae. The motor conducting velocities of the grafting segments wer e on average 47.2 m/s in ANG, 60.9 m/s in AG and 122.0m/s in normal controls. St imuli (5.0-10.0 mA, 0.2 ms, 1.9 Hz) to the right distal tibial nerves resulted in sensory-evoked potentials recorded from the cortical area in all the canines in ANG and AG groups. Axons regeneration and Schwann cells migration had reoccu pied the empty basal lamina tubes of the acellular allografting segments without excessive sign of inflammation. ANG and AG had similar nerve regeneration with massive large nerve fibers in the distal tibial nerves and vast motor end-plate in the target muscle. Conclusions The patterns of functional recovery and nerve regeneration tend to be similar 6 months after implantation in the canines, in which a 5.0 cm gap in the continuity of the sciatic nerve is repaired by either chemical acellular nerve allografting or autografting.
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Objective To investigate the apoptosis rate of neurons in vitro among the primary culture cells isolated from rat spinal cords before and after injury. Methods The spinal cord neurons of Wistar rats at 14-day gestation were isolated and cultured. The neuronal processes were then injured by cutting. At different time points after injury, TUNEL method was employed to detect the apoptotic neurons. Results Before injury, there was almost no apoptotic neuron. However, a large amount of apoptotic neurons were observed after the injury. The highest incidence of apoptosis appeared on the first day, and then it gradually reduced in the following days, but increased in amount again on the seventh day. Conclusion The results of the present experiment reveal the regularity of apoptosis of neurons before and after injury, and it provides a platform for further research regarding therapeutic intervention in the treatment of spinal cord injury.