Modig J, Samuelsson T, Sandin R
Acta Chir Scand. 1986 Oct;152:569-75.
The effects of treatment with PGE1 were evaluated in a porcine model of early adult respiratory distress syndrome induced by endotoxaemia. Spontaneously breathing pigs under ketamine anaesthesia were infused i.v. with E. coli endotoxin (10 micrograms X kg-1 X h-1) for 6 h. Thirteen pigs were given endotoxin, and 11 pigs were treated with a continuous infusion of PGE1, 0.25 microgram X kg-1 X min-1 for 4 h, beginning 2 h after start of endotoxin and established lung injury. Four pigs served as controls and receiving only PGE1 (0.25 microgram X kg-1 X min-1) during the whole observation period of 6 h. PGE1 treatment did not influence the decline in platelet and polymorphonuclear cell counts, whereas it markedly decreased the pulmonary hypertension induced by endotoxaemia. The increased extravascular lung water returned towards baseline after institution of PGE1. The increased venous admixture was not significantly influenced by PGE1. Treatment with PGE1 induced an exacerbated hypotensive state in the endotoxaemic animals primarily due to vasodilation. The decline in cardiac output and oxygen delivery noted in endotoxaemic pigs were not influenced by PGE1 and survival was not improved. Although one should be extremely careful in extrapolating these data to the clinical situation the results from the present study suggest the need for optimum volume replacement when starting PGE1 infusion in endotoxin-induced ARDS.
在内毒素血症诱导的成年早期呼吸窘迫综合征猪模型中评估了前列腺素E1(PGE1)的治疗效果。在氯胺酮麻醉下自主呼吸的猪静脉内输注大肠杆菌内毒素(10微克·千克⁻¹·小时⁻¹),持续6小时。13只猪接受内毒素,11只猪在内毒素输注开始并出现肺损伤2小时后开始连续输注PGE1,剂量为0.25微克·千克⁻¹·分钟⁻¹,持续4小时。4只猪作为对照,在整个6小时观察期内仅接受PGE1(0.25微克·千克⁻¹·分钟⁻¹)。PGE1治疗不影响血小板和多形核细胞计数的下降,然而它显著降低了内毒素血症诱导的肺动脉高压。PGE1应用后,血管外肺水增加量恢复至基线水平。静脉混合血增加未受到PGE1的显著影响。PGE1治疗在内毒素血症动物中导致了更严重的低血压状态,主要是由于血管扩张。内毒素血症猪中心输出量和氧输送的下降未受到PGE1的影响,生存率也未提高。尽管将这些数据外推至临床情况时应极其谨慎,但本研究结果表明在内毒素诱导的急性呼吸窘迫综合征中开始输注PGE1时需要进行最佳的容量补充。