Forsgren P, Modig J
Acta Chir Scand. 1986 Oct;152:561-8.
In a porcine model employing a continuous i.v. infusion of E. coli endotoxin the pathophysiology of early adult respiratory distress syndrome was studied with main emphasis on the early changes in lung mechanics and their relation to changes in pulmonary haemodynamics, gas exchange and extravascular lung water in intermittent positive pressure ventilated (IPPV) pigs under ketamine anaesthesia. Six animals served as controls and revealed no major physiological changes. Nine animals received endotoxin and developed significant changes in lung mechanics with increases in end-inspiratory pressure (32%), expiratory resistance (29%) and decrease in total dynamic lung compliance (27%). Changes in dynamic compliance and pulmonary haemodynamics displayed a 2-phase reaction. Venous admixture showed a rapid increase at with the increase in mean pulmonary arterial pressure (r = -0.8) and with the increase in venous admixture (r = -0.7). Extravascular lung water did not increase significantly. The decrease in dynamic compliance is most likely explained by peripheral airway constriction. A contributory factor might be pulmonary microvascular constriction with vascular stasis and mechanical compression of small airways. The increased venous admixture is best explained by a bronchiolar and microvascular constriction, i.e. a "dry" ventilation/perfusion inequality and not consequent to oedema. IPPV seems to counteract the increase in extravascular lung water.
在一个采用持续静脉输注大肠杆菌内毒素的猪模型中，研究了早期成人呼吸窘迫综合征的病理生理学，主要关注氯胺酮麻醉下间歇性正压通气（IPPV）猪的肺力学早期变化及其与肺血流动力学、气体交换和血管外肺水变化的关系。六只动物作为对照，未显示出重大生理变化。九只动物接受内毒素后，肺力学出现显著变化，吸气末压力增加（32%）、呼气阻力增加（29%），总动态肺顺应性降低（27%）。动态顺应性和肺血流动力学的变化呈现双相反应。静脉混合血随着平均肺动脉压的升高（r = -0.8）和静脉混合血的增加（r = -0.7）迅速增加。血管外肺水没有显著增加。动态顺应性降低最可能的原因是外周气道收缩。一个促成因素可能是肺微血管收缩伴血管淤滞以及小气道的机械性压迫。静脉混合血增加最好的解释是细支气管和微血管收缩，即“干性”通气/灌注不均，而非水肿所致。IPPV似乎能抵消血管外肺水的增加。
