Smith M E, Gunther R, Zaiss C, Demling R H
Arch Surg. 1982 Feb;117(2):175-80. doi: 10.1001/archsurg.1982.01380260045008.
The use of prostaglandins is currently undergoing clinical trials in respiratory failure accompanying sepsis. The effect of prostaglandin E1 (PGE1) and prostacyclin (PGI2) infusion on endotoxin-induced lung injury, with attention to interstitial fluid flux (QL), pulmonary vascular pressure (Ppa), leukocytes, platelets, and release of the lysosomal enzyme beta-glucuronidase, was investigated. A chronic lung lymph fistula model in sheep was used. Seven sheep alternately received Escherichia coli endotoxin and endotoxin plus PGE at a dosage of 1 microgram/kg/min. Six sheep received PGI2 (0.2 microgram/kg/min) instead of PGE1. Both PGE1 and PGI2 decreased the pulmonary hypertension and the interstitial edema produced by endotoxin primarily through their vasodilatory properties. Prostacyclin seemed to have an additional membrane-stabilizing effect. A rebound increase in QL, Ppa, and platelets occurred when PGE1 or PGI2 infusion was discontinued.
目前，前列腺素正在伴随脓毒症的呼吸衰竭中进行临床试验。研究了输注前列腺素E1（PGE1）和前列环素（PGI2）对内毒素诱导的肺损伤的影响，重点关注间质液通量（QL）、肺血管压力（Ppa）、白细胞、血小板以及溶酶体酶β-葡萄糖醛酸酶的释放。使用了绵羊慢性肺淋巴瘘模型。7只绵羊交替接受大肠杆菌内毒素以及剂量为1微克/千克/分钟的内毒素加PGE。6只绵羊接受PGI2（0.2微克/千克/分钟）而非PGE1。PGE1和PGI2均主要通过其血管舒张特性降低了内毒素所致的肺动脉高压和间质水肿。前列环素似乎还有额外的膜稳定作用。当停止输注PGE1或PGI2时，QL、Ppa和血小板出现反弹性增加。
