Bredthauer Andre, Lehle Karla, Scheuerle Angelika, Schelzig Hubert, McCook Oscar, Radermacher Peter, Szabo Csaba, Wepler Martin, Simon Florian
Department of Anesthesiology, University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany.
Institute of Anesthesiological Pathophysiology and Process Engineering, University Hospital Ulm, Helmholtzstraße 8/1, 89081, Ulm, Germany.
Intensive Care Med Exp. 2018 Oct 24;6(1):44. doi: 10.1186/s40635-018-0209-y.
In rodents, intravenous sulfide protected against spinal cord ischemia/reperfusion (I/R) injury during aortic balloon occlusion. We investigated the effect of intravenous sulfide on aortic occlusion-induced porcine spinal cord I/R injury.
Anesthetized and mechanically ventilated "familial hypercholesterolemia Bretoncelles Meishan" (FBM) pigs with high-fat-diet-induced hypercholesterolemia and atherosclerosis were randomized to receive either intravenous sodium sulfide 2 h (initial bolus, 0.2 mg kg body weight (bw); infusion, 2 mg kg bw h; n = 4) or vehicle (sodium chloride, n = 4) prior to 45 min of thoracic aortic balloon occlusion and for 8 h during reperfusion (infusion, 1 mg kg bw h). During reperfusion, noradrenaline was titrated to maintain blood pressure at above 80% of the baseline level. Spinal cord function was assessed by motor evoked potentials (MEPs) and lower limb reflexes using a modified Tarlov score. Spinal cord tissue damage was evaluated in tissue collected at the end of experiment using hematoxylin and eosin and Nissl staining.
A balloon occlusion time of 45 min resulted in marked ischemic neuron damage (mean of 16% damaged motoneurons in the anterior horn of all thoracic motor neurons) in the spinal cord. In the vehicle group, only one animal recovered partial neuronal function with regain of MEPs and link motions at each time point after deflating. All other animals completely lost neuronal functions. The intravenous application of sodium sulfide did not prevent neuronal cell injury and did not confer to functional recovery.
In a porcine model of I/R injury of the spinal cord, treatment with intravenous sodium sulfide had no protective effect in animals with a pre-existing arteriosclerosis.
在啮齿动物中，静脉注射硫化物可在主动脉球囊闭塞期间预防脊髓缺血/再灌注（I/R）损伤。我们研究了静脉注射硫化物对主动脉闭塞诱导的猪脊髓I/R损伤的影响。
将麻醉并机械通气的“布列塔尼梅山家族性高胆固醇血症”（FBM）猪，这些猪因高脂饮食诱导患有高胆固醇血症和动脉粥样硬化，随机分为两组，在胸主动脉球囊闭塞45分钟前及再灌注8小时期间（输注速度为1mg/kg体重·小时），一组接受静脉注射硫化钠2小时（初始推注剂量为0.2mg/kg体重；输注速度为2mg/kg体重·小时；n = 4），另一组接受赋形剂（氯化钠，n = 4）。在再灌注期间，滴定去甲肾上腺素以将血压维持在基线水平以上80%。使用运动诱发电位（MEP）和改良的塔尔洛夫评分评估下肢反射来评估脊髓功能。使用苏木精和伊红以及尼氏染色对实验结束时收集的组织中的脊髓组织损伤进行评估。
45分钟的球囊闭塞时间导致脊髓中明显的缺血性神经元损伤（所有胸段运动神经元前角中平均16%的运动神经元受损）。在赋形剂组中，只有一只动物在放气后的每个时间点恢复了部分神经元功能，MEP恢复且有连接运动。所有其他动物完全丧失了神经元功能。静脉注射硫化钠并未预防神经元细胞损伤，也未实现功能恢复。
在猪脊髓I/R损伤模型中，静脉注射硫化钠治疗对已有动脉硬化的动物没有保护作用。
