利用负压通气的离休兔肺灌流模型研究高浓度氯气（5000ppm）急性染毒引起肺损伤及肺水肿的病理生理机理．方法：9只自体血灌注、负压通气（吸入950mL／LO2及50mL／LCO2）的离体兔肺灌流模型为对照组；10只吸入5000ppm的氯气，染毒20min．在控制回流压力的情况下，动态监测灌流压力、肺重量的变化；荧光光度法测定灌流血液血浆中组织胺、5-羟色胺含量；测定肺湿／干重比值等．结果：在控制回流压力与灌流液流速（133．3mL／min）不变的情况下，染毒10min后，与未染毒的离体灌流肺相比肺重量迅速增加继而灌流压力开始增高；灌流液血球压积值显著增高；灌流血液的血浆中组织胺含量增高，而5-羟色胺含量未见明显增加；肺湿／干重比值显著增加．外观见明显肺水肿、大量粉红色泡沫自气管涌出；光镜见肺充血、肺水肿及肺气肿．结论：高浓度氯气染毒可导致肺水肿，其发生机制主要是由于微血管渗透性的增加，而后者可能与组织胺的增加有关． The pathophysiological mechanism of lung injury and pulmonary edema induced by acute exposure to high concentration chlorine (5000ppm) was studied by using negative pressure ventilation in reperfused rabbit lung perfusion model. Methods: Nine rabbit models of autologous blood perfusion and negative pressure ventilation (inhalation of 950mL / LO2 and 50mL / LCO2) were used as the control group. Ten rats inhaled 5000ppm chlorine for 20min. Under the condition of controlling the reflux pressure, the change of perfusion pressure and lung weight was monitored dynamically. The histamine and serotonin in perfusion blood plasma were determined by fluorophotometry. The wet / dry lung weight ratio was measured. RESULTS: After controlling the reflux pressure and the flow rate of the perfusate (133.3mL / min), the lung weight rapidly increased and then the perfusion pressure began to increase compared with the non-exposed perfusion lungs after 10min exposure. The perfusion The hematocrit value increased significantly. The content of histamine in plasma of perfused blood increased, while the content of 5-hydroxytryptamine was not increased obviously. The wet / dry weight ratio of lung increased significantly. The appearance of obvious pulmonary edema, a large number of pink foam from the tracheal gush; light microscopy see pulmonary congestion, pulmonary edema and emphysema. Conclusion: High concentration chlorine exposure can cause pulmonary edema. Its mechanism is mainly due to the increase of microvascular permeability, while the latter may be related to the increase of histamine.