Förster W
Z Gesamte Inn Med. 1985 Apr 15;40(8):217-21.
The pathogenesis of shock is discussed on the basis of important results from world literature under the special point of view of the significance of eicosanoids. It results from a lower mortality of shock animals with a diet poor in polyunsaturated fatty acids and a specifically increased release of arachidonic acid as prostaglandin precursor in shock animals. Of particular importance is an increased formation of thromboxane B2 (TXB2). It this formation is specifically inhibited, the survival rate increases, the decrease of blood pressure is reduced, also the increase of the plasma-cathepsin-D-activity and of the myocardial depressant factor and the increased formation of microthrombi in renal glomeruli of shock animals. Also in patients who survived the shock the TXB2-values were only 1/10 of the values in decreased shock patients. Another therapeutic way is the infusion of prostacyclin which leads to a specific increase of the arterial blood supply of the liver and the superior mesenteric artery and also increases the ATP and creatine phosphate level. The importance of the findings of animal experiments for the pathogenesis and therapy in patients is discussed.
基于世界文献的重要研究成果,从类二十烷酸的重要性这一特殊角度探讨了休克的发病机制。这源于食用多不饱和脂肪酸含量低的食物的休克动物死亡率较低,以及休克动物体内作为前列腺素前体的花生四烯酸释放量特别增加。特别重要的是血栓素B2(TXB2)的生成增加。如果这种生成受到特异性抑制,存活率会提高,血压下降会减轻,休克动物血浆组织蛋白酶-D活性、心肌抑制因子的增加以及肾小球微血栓形成的增加也会减轻。在休克后存活的患者中,TXB2值也仅为休克病情加重患者的1/10。另一种治疗方法是输注前列环素,这会导致肝脏和肠系膜上动脉的动脉血液供应特异性增加,同时也会提高三磷酸腺苷(ATP)和磷酸肌酸水平。文中还讨论了动物实验结果对患者发病机制和治疗的重要性。