Arrieta O, Ortiz-Reyes A, Rembao D, Calvillo M, Rivera E, Sotelo J
Neuroimmunology Unit and Experimental Pathology Laboratory, Instituto Nacional de Neurología y Neurocirugía and Universidad Nacional Autónoma de México.
Int J Exp Pathol. 1999 Feb;80(1):11-6. doi: 10.1046/j.1365-2613.1999.00085.x.
Mortality caused by septic shock in experimental animals is reduced by thalidomide, an inhibitor of tumour necrosis factor alpha. Another drug that could act on the pathophysiological mechanisms of septic shock is pentoxifylline, an inhibitor of platelet aggregation that increases the flexibility of the erythrocyte membrane and has fibrinolytic activity. We studied the effect of pentoxifylline alone and combined with thalidomide in septic shock; 97 NIH mice were injected with lipopolysaccharides of Salmonella abortus equi and D galactosamine. Animals were separated in 4 groups; group A (n = 20) was used as control, group B (n = 15) received thalidomide 50 mg/kg, group C (n = 20) received pentoxifylline 40 mg/kg, and group D (n = 15) received thalidomide plus pentoxifylline. Mortality was recorded every hour. Additionally, 5 animals from each group were sacrificed 8 h after the induction of septic shock for histological analysis of heart, lung, brain, kidney, small intestine, adrenal glands and liver. Microscopic findings were rated as absent, mild, moderate and severe damage. In control animals histological analysis showed intense haemorrhage and necrosis in all organs studied. When compared with controls, treatment with pentoxifylline plus thalidomide reduced mortality (P < 0.03). The tissue damage was less severe in animals from the groups that received pentoxifylline or pentoxifylline plus thalidomide (P < 0.05). Pentoxifylline seems to potentiate the beneficial effects of thalidomide, reducing mortality and attenuating the pathological changes produced by septic shock.
沙利度胺是一种肿瘤坏死因子α抑制剂,可降低实验动物因感染性休克导致的死亡率。另一种可作用于感染性休克病理生理机制的药物是己酮可可碱,它是一种血小板聚集抑制剂,可增加红细胞膜的柔韧性并具有纤溶活性。我们研究了己酮可可碱单独使用以及与沙利度胺联合使用对感染性休克的影响;将97只NIH小鼠注射马流产沙门氏菌和D - 半乳糖胺的脂多糖。动物被分为4组;A组(n = 20)用作对照,B组(n = 15)接受50 mg/kg沙利度胺,C组(n = 20)接受40 mg/kg己酮可可碱,D组(n = 15)接受沙利度胺加己酮可可碱。每小时记录死亡率。此外,在感染性休克诱导8小时后,每组处死5只动物,用于对心脏、肺、脑、肾、小肠、肾上腺和肝脏进行组织学分析。显微镜检查结果分为无、轻度、中度和重度损伤。在对照动物中,组织学分析显示在所有研究的器官中均有严重出血和坏死。与对照组相比,己酮可可碱加沙利度胺治疗可降低死亡率(P < 0.03)。接受己酮可可碱或己酮可可碱加沙利度胺组的动物组织损伤较轻(P < 0.05)。己酮可可碱似乎可增强沙利度胺的有益作用,降低死亡率并减轻感染性休克所产生的病理变化。