Linhardt G E, Trump B F, Jones R T
Adv Shock Res. 1980;3:175-86.
In order to determine if pharmacological intervention would modify the morphological alterations that we previously observed in the human liver in a rat hypovolemic shock model, male Sprague-Dawley rats were bled to a mean arterial pressure of 40 torr for 30 minutes. Following the shock period, animals were injected with either dopamine-HCl (30 micrograms/kg/min), glucagon (50 micrograms/kg/min) or methylprednisolone sodium succinate (30 mg/kg/min) over a 30-minute period. Following treatment, the shed blood was returned. Animals were killed at either 1 or 48 hours, a wedge biopsy of the liver was taken for morphological study, and a blood sample was taken for the determination of serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT). Alterations in the untreated shock controls were consistent with those seen in the human liver by ultrastructural study in cases of mild to moderate shock. The most prominent alteration in the rat liver was the formation of autophagic vacuoles at 1 hour, while at 48 hours there was an increase in residual bodies with a decrease in autophagic vacuoles in both glucagon treated and in untreated controls. While dopamine and methylprednisolone significantly reduced the number of autophagic vacuoles and residual bodies in the animals studied, SGOT levels were increased in the glucagon and methylprednisolone treated animals at 48 hours and SGPT levels were increased only in the glucagon-treated animals at the same time period. Results suggest that methylprednisolone or dopamine prevent sublethal alterations in the rat liver in moderate hypovolemic shock.
为了确定药物干预是否会改变我们先前在大鼠低血容量性休克模型中观察到的人类肝脏形态学改变,将雄性Sprague-Dawley大鼠放血至平均动脉压40托,持续30分钟。休克期过后,在30分钟内给动物注射盐酸多巴胺(30微克/千克/分钟)、胰高血糖素(50微克/千克/分钟)或琥珀酸钠甲泼尼龙(30毫克/千克/分钟)。治疗后,将放出的血液回输。在1小时或48小时处死动物,取肝脏楔形活检组织进行形态学研究,并采集血样测定血清谷草转氨酶(SGOT)和血清谷丙转氨酶(SGPT)。未经治疗的休克对照组的改变与轻度至中度休克病例中人类肝脏超微结构研究所见一致。大鼠肝脏最显著的改变是在1小时时形成自噬泡,而在48小时时,胰高血糖素治疗组和未治疗的对照组中残留小体增加,自噬泡减少。虽然多巴胺和甲泼尼龙显著减少了所研究动物的自噬泡和残留小体数量,但在48小时时,胰高血糖素和甲泼尼龙治疗组的SGOT水平升高,同期仅胰高血糖素治疗组的SGPT水平升高。结果表明,甲泼尼龙或多巴胺可预防中度低血容量性休克大鼠肝脏的亚致死性改变。