Ebata T, Asaishi K, Hiraike N, Yamamoto Y, Hasegawa I, Minamida H, Hayasaka H
First Department of Surgery, Sapporo Medical College, Japan.
Nihon Geka Gakkai Zasshi. 1989 Sep;90(9):1378-81.
From 1975 to 1987, we had 56 patients of septic shock in the Department of Surgery. Multiple organ failure occurred in many septic patients. Glucocorticoids inhibited the secretion of chemical mediators (histamine, serotonin and bradykinin) and then prevented septic shock. Intravenous administration of dexamethasone showed no change in amounts of leukotrienes (LTC4, LTD4, LTE4) in venous blood in peritonitis rats. Dexamethasone treatment of septic rats corrected FDP and nearly normalized PEP values. When glucocorticoid was given intravenously at the time of cecal incision, PFKase, PKase, G6Pase and PEPCK were stimulated, respectively. Protease inhibitor FUT-175 was infused in 5% dextrose (0.1mg/ml/hr) in septic rats. Survival time was 12.1 +/- 2.3 hour in FUT-175 group and 6.6 +/- 1.1 hr without FUT-175. In FUT-175 injected rats G6P decreased by 20%, FDP increased 50% and lactate doubled. PEP levels increased 30% above peritonitis values. The amounts of leukotrienes (LTC4, LTD4, LTE4) in venous blood were gradually decreased by pretreatment with the specific 5-lipoxygenase inhibitor AA-861 after peritonitis. Specific treatments in septic shock should be instituted administration of glucocorticoid, antibiotics, protease inhibitor and lipoxygenase inhibitor. The importance of septic shock as a factor contributing to organ failure must be acknowledge. We believe that the prompt and efficacious treatment of septic shock is the best therapy.
1975年至1987年期间，我们外科有56例感染性休克患者。许多感染患者发生了多器官功能衰竭。糖皮质激素抑制化学介质（组胺、5-羟色胺和缓激肽）的分泌，从而预防感染性休克。静脉注射地塞米松后，腹膜炎大鼠静脉血中的白三烯（LTC4、LTD4、LTE4）量无变化。地塞米松治疗感染大鼠可纠正纤维蛋白降解产物（FDP）并使磷酸烯醇式丙酮酸羧激酶（PEPCK）值接近正常。在盲肠切开时静脉给予糖皮质激素，磷酸果糖激酶（PFKase）、丙酮酸激酶（PKase）、葡萄糖-6-磷酸酶（G6Pase）和PEPCK分别受到刺激。在感染大鼠中，蛋白酶抑制剂FUT-175以5%葡萄糖（0.1mg/ml/小时）输注。FUT-175组的生存时间为12.1±2.3小时，未使用FUT-175组为6.6±1.1小时。在注射FUT-175的大鼠中，G6P下降20%，FDP增加50%，乳酸增加一倍。PEP水平比腹膜炎时的值增加30%。腹膜炎后用特异性5-脂氧合酶抑制剂AA-861预处理可使静脉血中的白三烯（LTC4、LTD4、LTE4）量逐渐减少。感染性休克的特异性治疗应包括糖皮质激素、抗生素、蛋白酶抑制剂和脂氧合酶抑制剂的应用。必须认识到感染性休克作为导致器官功能衰竭因素的重要性。我们认为，及时有效地治疗感染性休克是最佳疗法。
