大肠杆菌内毒素所致肺血管收缩部位及山莨菪碱的作用

将动、静脉阻断法用于恒速灌流的在体山羊左肺,使其总压力降区分为动脉端、静脉端及中间段三部分。大肠杆菌内毒素主要升高肺静脉端压力降及肺毛细血管压;山莨菪碱可显著缓解内毒素所致的改变,但对正常肺血管各段压力降无明显影响。5-羟色胺主要升高肺动脉端压力降,对肺静脉端及毛细血管压无明显影响。去甲肾上腺素及组胺主要升高肺静脉端压力降及肺毛细血管压,但对肺动脉端无明显影响。去甲肾上腺素和组胺可能介导内毒素性肺动脉高压。

Site of Endotoxic Pulmonary Vasoconstriction and the Effect of Anisodamine

Using arterial and venous occlusion techniques in an in situ, isolated left goat lung preparation, the total arteriovenous pressure drop across the lung was partitioned vertically into pressure drops across the relatively indistensable arteries (delta Pa) and veins (delta Pv) and the middle distensible vessels (delta Pm). Endotoxin primarily increased delta Pv and Pc. Anisodamine only showed a slight effect on pressure drops in different segment under normal conditions. It could attenuate the endotoxin effect however. Serotonin mainly increased delta Pa and showed no effect on delta Pv and delta Pm. Norepinephrine and histamine increased delta Pv and Pc while it showed almost no effect on delta Pa. It is possible that the norepinephrine and histamine mediate the pulmonary hypertension caused by endotoxin.