目的:观察抑肽酶预处理对兔脊髓缺血再灌注损伤的影响,为临床应用抑肽酶治疗脊髓缺血再灌注损伤提供实验依据。方法:6月龄国产大耳白兔39只,随机分为A组(15只)、B组(15只)和C组(9只)。A、B组动物于左肾动脉下用主动脉环扎器环扎腹主动脉,缺血60min后开放,再灌注24h。A组于缺血前10min静脉注射抑肽酶3×107IU/kg,继而用Graseby3500微量泵持续注入抑肽酶1×107IU/(kg·h)至处死动物时;B组用生理盐水代替A组的抑肽酶,其余同A组;C组只暴露不夹闭腹主动脉,不给药。A、B组缺血前,缺血5、10、20、60min及再灌注后8h、24h,C组相应时间点,测定各组皮层体感诱发电位(CSEP)。A、B组缺血前,缺血再灌注后8h、24h,C组相应时间点,处死动物,取L2～L4脊髓行一氧化氮(NO)及一氧化氮合酶(NOS)测定,取L3～L4脊髓灰质切片进行组织学检查,观察神经元形态变化。结果:A、B两组缺血5min时CSEP的P1波和N1波潜伏期较缺血前延长、波幅降低(P<0.05),缺血20min时两波潜伏期及波幅消失,缺血再灌注后8h两波潜伏期及波幅有所恢复,但较缺血前及缺血后5min、10min时明显延长和降低(P<0.01),缺血再灌注后24h两波潜伏期及波幅较前面各时间点延长和降低(P<0.01);缺血再灌注后8h、24h,A组较B组P1波和N1波潜伏期短、波峰高(P<0.05),而C组较A、B组潜伏期短、波峰高(P<0.01)。A、B两组NO、总NOS及诱导型NOS(iNOS)在缺血再灌注后8h明显升高,24h时更高(P<0.05),在缺血再灌注后8h、24h时A组的NO、总NOS及iNOS较B组低(P<0.01)。各时间点C组P1波和N1波潜伏期及波幅不变,NO、总NOS及iNOS量均不变(P>0.05)。A、B组脊髓缺血再灌注后神经元均有损伤,但在再灌注后8h、24h时A组神经元损伤程度均较B组为轻;C组神经元正常。结论:抑肽酶预处理可以改善脊髓缺血再灌注早期的CSEP,减少NO含量,从而减少缺血再灌注损伤。 OBJECTIVE: To observe the effect of aprotinin preconditioning on spinal cord ischemia-reperfusion injury in rabbits and provide experimental evidence for the clinical application of aprotinin in the treatment of spinal cord ischemia-reperfusion injury. Methods: 39 domestic white rabbits aged 6 months were randomly divided into group A (n = 15), group B (n = 15) and group C (n = 9). A, B group of animals under the left renal artery cerclage aortic ring cerclage abdominal aorta ischemia 60min after opening, reperfusion 24h. In group A, aprotinin 3 × 107IU / kg was intravenously injected 10 min before ischemia, then aprotinin 1 × 107IU / (kg · h) was continuously infused with Graseby 3500 pump to kill animals. In group B, saline was used instead of group A Of the aprotinin, the rest with the A group; C group only unclamped abdominal aorta, not administered. Groups A, B before ischemia, ischemia 5,10,20,60 min and 8h, 24h after reperfusion, C group corresponding time points, the determination of cortical somatosensory evoked potentials (CSEP). Animals in group A and B were pre-ischemic, 8h and 24h after ischemia / reperfusion, and animals in group C were sacrificed at the corresponding time points. The levels of nitric oxide (NO) and nitric oxide synthase (NOS) were measured in L2 ~ L4 spinal cord L3 ~ L4 spinal cord histological examination to observe the morphological changes of neurons. Results: The latency and amplitude of P1 wave and N1 wave of CSEP were prolonged and the amplitude of CS wave was lower (P <0.05) at 5 minutes after ischemia in both groups A and B. The latency and amplitude of two waves disappeared at 20 minutes after ischemia, The latency and amplitude of the two waves recovered, but were significantly longer and lower than those before 5min and 10min after ischemia (P <0.01). The latency and amplitude of two waves 24h after ischemia-reperfusion were longer than those before (P <0.01). At 8h and 24h after ischemia-reperfusion, the latency of P1 wave and N1 wave in group A were shorter than those in group B, and the wave peak was higher (P <0.05), while the latency in group C was shorter than that in group A and B (P <0.01). The levels of NO, total NOS and iNOS in A and B groups increased significantly at 8h after ischemia-reperfusion and higher at 24h (P <0.05), while at 8h and 24h after ischemia-reperfusion, NO, total NOS and iNOS were lower than those in group B (P <0.01). The latency and amplitude of P1 wave and N1 wave in group C remained unchanged at all time points, and the levels of NO, total NOS and iNOS were unchanged (P> 0.05). Neurons were damaged after spinal cord ischemia-reperfusion in groups A and B, but neurons in group A were lighter than those in group B at 8 and 24 hours after reperfusion. Neurons in group C were normal. Conclusion: Pretreatment with aprotinin can improve the CSEP in the early stage of spinal cord ischemia-reperfusion, decrease the content of NO, and reduce the damage of ischemia-reperfusion.