Clinic for Horses, University of Veterinary Medicine Hannover, Hannover, Germany.
Department of Biochemistry, University of Veterinary Medicine Hannover, Hannover, Germany.
BMC Vet Res. 2021 Apr 26;17(1):175. doi: 10.1186/s12917-021-02877-y.
Ischaemic postconditioning (IPoC) refers to brief periods of reocclusion of blood supply following an ischaemic event. This has been shown to ameliorate ischaemia reperfusion injury in different tissues, and it may represent a feasible therapeutic strategy for ischaemia reperfusion injury following strangulating small intestinal lesions in horses. The objective of this study was to assess the degree cell death, inflammation, oxidative stress, and heat shock response in an equine experimental jejunal ischaemia model with and without IPoC.
In this randomized, controlled, experimental in vivo study, 14 horses were evenly assigned to a control group and a group subjected to IPoC. Under general anaesthesia, segmental ischaemia with arterial and venous occlusion was induced in 1.5 m jejunum. Following ischaemia, the mesenteric vessels were repeatedly re-occluded in group IPoC only. Full thickness intestinal samples and blood samples were taken at the end of the pre-ischaemia period, after ischaemia, and after 120 min of reperfusion. Immunohistochemical staining or enzymatic assays were performed to determine the selected variables.
The mucosal cleaved-caspase-3 and TUNEL cell counts were significantly increased after reperfusion in the control group only. The cleaved-caspase-3 cell count was significantly lower in group IPoC after reperfusion compared to the control group. After reperfusion, the tissue myeloperoxidase activity and the calprotectin positive cell counts in the mucosa were increased in both groups, and only group IPoC showed a significant increase in the serosa. Tissue malondialdehyde and superoxide dismutase as well as blood lactate levels showed significant progression during ischaemia or reperfusion. The nuclear immunoreactivity of Heat shock protein-70 increased significantly during reperfusion. None of these variables differed between the groups. The neuronal cell counts in the myenteric plexus ganglia were not affected by the ischaemia model.
A reduced apoptotic cell count was found in the group subjected to IPoC. None of the other tested variables were significantly affected by IPoC. Therefore, the clinical relevance and possible protective mechanism of IPoC in equine intestinal ischaemia remains unclear. Further research on the mechanism of action and its effect in clinical cases of strangulating colic is needed.
缺血后处理(IPoC)是指在缺血事件后短暂地再次阻断血液供应。这已被证明可改善不同组织的缺血再灌注损伤,并且对于马的绞窄性小肠损伤后的缺血再灌注损伤,它可能代表一种可行的治疗策略。本研究的目的是评估在有和没有 IPoC 的情况下,马实验性空肠缺血模型中的细胞死亡、炎症、氧化应激和热休克反应的程度。
在这项随机、对照、体内实验研究中,14 匹马被平均分配到对照组和 IPoC 组。在全身麻醉下,用动脉和静脉闭塞法在 1.5 m 空肠上诱导节段性缺血。在缺血后,仅在 IPoC 组中重复再闭塞肠系膜血管。在缺血前、缺血后和再灌注 120 分钟时,采集全层肠组织样本和血液样本。通过免疫组织化学染色或酶测定法进行测定。
只有在对照组中,再灌注后黏膜裂解半胱天冬酶-3 和 TUNEL 细胞计数显著增加。与对照组相比,再灌注后 IPoC 组的裂解半胱天冬酶-3 细胞计数明显降低。再灌注后,两组的组织髓过氧化物酶活性和黏膜中钙卫蛋白阳性细胞计数均增加,只有 IPoC 组的浆膜中增加显著。组织丙二醛和超氧化物歧化酶以及血液乳酸水平在缺血或再灌注过程中均显著升高。再灌注过程中核热休克蛋白-70 的免疫反应性显著增加。这些变量在两组之间均无差异。空肠壁内神经节神经元细胞计数不受缺血模型的影响。
在接受 IPoC 的组中,凋亡细胞计数减少。其他测试变量均不受 IPoC 的显著影响。因此,IPoC 在马肠缺血中的临床相关性和可能的保护机制尚不清楚。需要进一步研究其作用机制及其在绞窄性疝的临床病例中的效果。