目的:探讨缺血后处理对不同缺血程度的兔睾丸缺血再灌注损伤的作用。方法:42只雄性大白兔随机分成对照组、缺血组(R1、R2、R3组)、后处理组(P1、P2、P3组),每组6只。缺血组、后处理组在超声监测下制成睾丸不同缺血程度模型:R1、P1组睾丸回声均匀,血流轻度减少;R2、P2组睾丸回声增粗,血流明显减少;R3、P3组睾丸出现片状或放射状低回声,血流信号消失。出现上述图像变化后,缺血组给予直接灌流,后处理组于恢复灌流前给予后处理措施,即再灌注30s/缺血30s,反复3次。再灌注前进行超声造影,3d后测定各组组织丙二醛(MDA)、超氧化物歧化酶(SOD)含量。HE染色后光镜下观察睾丸组织和病理学改变,并行Johnsen's评分和凋亡指数分析;电镜下观察睾丸组织超微结构。结果:再灌注前各造影参数速度参数(β)、峰值时间(TTP)、峰值基础强度差(PBD)、峰值减半时间(DT/2),R1与P1组比较均无显著差异(P〉0.05)、R2与P2组比较均无显著差异(P〉0.05)、R3与P3组无显影。MDA含量:R1与P1组比较有显著差异(P〈0.05),R2与P2组比较有显著差异(P〈0.05),R3与P3组比较无显著差异(P〉0.05)。SOD活性:R1与P1组比较有显著差异(P〈0.05),R2与P2组比较有显著差异(P〈0.05),R3与P3组比较无显著差异(P〉0.05)。Johnsen's评分:R1与P1组比较有显著差异(P〈0.05),R2与P2组比较无显著差异(P〉0.05),R3与P3组比较无显著差异(P〉0.05)。凋亡指数:R1与P1组比较有显著差异(P〈0.05),R2与P2组比较无显著差异(P〉0.05),R3与P3组比较无显著差异(P〉0.05)。电镜:P1组超微结构损伤程度较R1组轻,R2与P2组超微结构无明显差异,R3与P3组超微结构无明显差异。结论:缺血后处理可以减轻睾丸缺血再灌注损伤,但是受到缺血程度的影响,并且在病理学和生化学上的表现不一致?
Objective:To investigate the protective effect of ischemic postconditioning (IP) against different degrees of testicular ischemia-reperfusion (IR) injury in rabbits. Methods: Forty-two white male rabbits were equally randomized into 7 groups: a control, 3 IR (R1, R2 and R3), and 3 IP (P1, P2 and P3) groups. Testicular models of different degrees of ischemia were established in the IR and IP groups. Before reperfusion, ultrasonography showed homogeneous echoes with slightly decreased blood flow in R1 and P1, heterogeneous echoes with obviously decreased blood flow in R2 and P2, lamellar or fragmental low echo areas absent of blood flow signals in R3 and P3. Then the IR groups were directly subjected to perfusion, and the IP groups to 3 episodes of 30-second reperfusion followed by 30-second ischemia. All the groups underwent contrast-enhanced ultrasonography (CEUS) before reperfusion and, after 3 days, examined for the contents of malonaldehyde (MDA), superoxide dismutase (SOD) and histology, and observed for the pathological changes of the testicular tissue. Results: Before reperfusion, no significant differences were found in the CEUS parameters β, time-to- peak (TTP), peak-base intensity (PBD) and half of declining time (DT/2) between R1 and P1, R2 and P2, and R3 and P3 (P0.05). There were remarkable differences in MDA and SOD between R1 and P1, and R2 and P2 (P0.05), but not between R3 and P3 (P0.05). Johnsen's score, apoptosis index and ultrastructure showed marked differences between R1 and P1 (P0.05) but not between R2 and P2, and R3 and P3 (P0.05). Conclusion: IP can attenuate IR-induced testis injury, but the effect varies with the degree of ischemia, and its pathological manifestation differs from the biochemical one.