重度心肌挫伤的发病机制

Experimental study on mechanisms of severe myocardial contusion in rabbits

目的： 探讨兔重度心肌挫伤发病机制． 方法： 新西兰兔３２只，随机平分成两组：重度心肌挫伤组（实验组）和伪撞击组（对照组）． 实验后２４ ｈ 检测血液流变学、血清ＩＬ－８含量、心肌含水量和心肌中性粒细胞（ＰＭＮ）浸润． 结果： 与对照组比较，实验组全血粘度、红细胞聚集指数、红细胞压积、血浆纤维蛋白原、Ｃａｓｓｏｎ 屈服值、红细胞沉降率均非常显著升高；ＩＬ－８含量、受创的心肌含水量和心肌ＰＭＮ浸润数均显著增加．结论： 血液流变学异常、ＩＬ－８含量升高及其所介导的ＰＭＮ浸润增加，共同参与了兔重度心肌挫伤后心肌水肿和继发性心肌损伤的发生和发展过程．

AIM: To investigate the mechanism of severe myocardial contusion in rabbits. METHODS: New Zealand rabbits were randomly divided into two groups: severe myocardial contusion group (experimental group) and sham impact group (control group). Sixteen animals were included in each group. Hemorrheological parameters, interlecukin 8 (IL 8) in plasma, the contents of cardiac water and neutrophil (PMN) infiltration in the contused myocardium were observed at 24h following the experiment. RESULTS: Com pared with those in the control group, the hemorrheological parameters in the experimental group, including ηb, EAI, HCT, Fib, Γy and ESR, were significantly increased. The contents of IL 8 in plasma, the contents of cardiac water and PMN infiltration in contused myocardium were also significantly increased. CONCLUSION: Our study suggests that the hemorrheological disorder, the increase of IL 8 in plasma, and PMN infiltration in the contused myocardium may contribute to the development of cardiac edema and secondary myocardial damage following severe myocardial contusion in rabbits.