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目的:探讨实验性急性肾功能衰竭 (Acuterenalfailure, ARF)兔血小板聚集功能、PGI2、TXA2、内皮素(Endothelins,ET)的变化与心肌组织形态学变化的关系。方法:实验分为 2组。对照组 (8只 ):用生理盐水 10ml/ 行后肢肌肉内加压注射。ARF组(12只):用 50%甘油 10mg/kg后肢肌肉内加压注射。检测各组不同时相血小板聚集功能等指标。结果: 2h、24hARF组与对照组比较:ARF组血小板聚集性明显增高(P<0. 01),TXA2、ET明显升高(P<0. 01), 6 Keto PGF1a明显降低(P<0. 01)。心肌组织出现严重的缺血性损害,主要为:心肌细胞弥漫性变性、心肌纤维间质水肿、血管周围水肿等。结论: ARF时血小板聚集性改变以及血管活性物质和氧自由基增高可能是造成心肌组织缺血性损害的直接原因之一。
Objective: To investigate the relationship between platelet aggregation, PGI2, TXA2 and endothelins (ET) and myocardial histopathological changes in experimental acute renal failure (ARF). Methods: The experiment was divided into two groups. Control group (8): with normal saline 10ml / line hindlimb muscle injection. ARF group (n = 12): intramuscular injection with 50% glycerol 10mg / kg hindlimb. The indexes of platelet aggregation in different groups at different time were detected. Results: Compared with the control group, the platelet aggregation of ARF group was significantly increased at 2h and 24h (P <0.01), the levels of TXA2 and ET were significantly increased (P <0.01), and Keto PGF1a was significantly decreased (P <0. 01). Myocardial tissue with severe ischemic damage, mainly as: diffuse myocardial cell degeneration, myocardial fibrosis, interstitial edema, perivascular edema and so on. CONCLUSIONS: Changes in platelet aggregation and increased levels of vasoactive substances and oxygen free radicals during ARF may be one of the direct causes of myocardial ischemic damage.