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本研究首次应用制动应激的力法,建立了家兔非创伤肺脂肪栓塞的实验模型。同时测定了左、右心血肝素后血浆脂蛋白酯酶(PHP-LPL)活性和游离脂肪酸(FFA)浓度。结合血浆儿茶酚胺的测定、血气分析、肺形态学(包括超微结构)和组织化学的研究,探讨了肺脂肪栓塞的发生机理。实验观察到,制动应激5h可造成成年家兔肺血管内脂肪栓塞,同时伴有肺环循中PHP-LPL活性和FFA浓度增高,低碳酸血症、及肺泡表面活性物质不足的倾向。结果提示,应激时的内环境紊乱,足以造成肺脂肪栓塞,而无须骨折等机械因素的参与。
In this study, we first applied the method of braking stress to establish an experimental model of noninvasive pulmonary fat embolism in rabbits. Plasma lipoprotein lipase (PHP-LPL) activity and free fatty acid (FFA) concentrations were measured simultaneously with left and right heparinized blood. Combined with the determination of plasma catecholamines, blood gas analysis, lung morphology (including ultrastructure) and histochemistry, the mechanism of pulmonary embolism was discussed. It has been observed experimentally that the 5h braking stress can cause pulmonary vascular fat embolism in adult rabbits with a tendency of increasing PHP-LPL activity and FFA concentration, hypocapnia, and insufficient alveolar surfactant in pulmonary circulation. The results suggest that the internal environment during stress disorder, enough to cause pulmonary fat embolism, without the need for mechanical factors such as fractures involved.