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本研究旨在探讨肝微循环障碍在病毒所致肝损伤发生中的作用。实验Ⅰ,麻疹活疫苗同时注入家兔门静脉及耳缘静脉,24小时快速放血处死,立即取肝固定送病理检查。光镜下可见小血管扩张瘀滞,红细胞粘集贴壁、纤维蛋白血小板构成之微血栓形成等严重微循环障碍的改变。同时可见肝细胞变性、小灶状坏死及GPT(血清谷丙转氨酶)等也明显升高。如先给予山莨菪碱,GPT等升高受到明显抑制。实验Ⅱ,麻疹活疫苗仅单独注入门静脉,24小时GPT并不升高,仅门脉血管对静注去甲肾上腺素的收缩反应性上升。实验Ⅲ,麻疹活疫苗仅注入耳缘静脉,24小时GPT也不升高,但血小板粘附功能增强。结果提示:(1)在病毒感染中肝血管收缩反应性上升及血小板粘附功能增强是肝微循环障碍发生的基础。(2)肝微循环障碍是病毒所致肝损伤的机理之一。(3)山茛菪碱是防治病毒性肝损伤的有效药物。
The purpose of this study was to investigate the role of hepatic microcirculatory disorders in the development of liver damage caused by the virus. In experiment I, the live measles vaccine was injected into the portal vein and ear veins of rabbits at the same time. The animals were sacrificed by rapid blood expulsion within 24 hours, and the livers were fixed immediately for pathological examination. Under microscopy, changes in small microvascular vasodilatation, erythrocyte adhesion and adherence, and microthrombus formation of fibrin platelets were observed. At the same time, liver cell degeneration, focal necrosis, and GPT (serum alanine aminotransferase) were also significantly increased. If anisodamine is given first, elevation of GPT is significantly inhibited. In Experiment II, the live measles vaccine was injected into the portal vein alone, and GPT did not increase at 24 hours. Only portal vein blood vessels showed increased contractility to norepinephrine. In experiment III, the live measles vaccine was injected only into the ear vein, and 24-hour GPT did not increase, but the platelet adhesion function was enhanced. The results suggest that: (1) Increased hepatic vasoconstriction and enhanced platelet adhesion in viral infections are the basis of hepatic microcirculation. (2) Liver microcirculatory disturbance is one of the mechanisms of liver damage caused by virus. (3) Anisodamine is an effective drug for preventing viral liver damage.