淡水接近淹溺肺损伤的病理生理研究

Pathophysiological study of lung injury in fresh water near downing

用 Carlen 管隔开左右肺,仅向右肺灌入淡水(25 ml/kg),观察淹溺后导致直接(右肺)和间接(左肺)肺损伤的病理变化,探讨 TNF,TXB_2,ACE 等介质在淹溺后肺损伤的作用。结果表明,淡水淹溺的直接和间接作用都可以引起肺损害。淹溺后,肺细胞表现为进行性损伤;1型肺上皮细胞出现损伤变化较Ⅱ型肺上皮细胞早;血气屏障破坏是喷射性肺水肿的病理学基础;TXB_2和 ACE 都参与于淹溺后肺损伤作用,但它们不是淹溺后肺损伤的标志;TNF 不是淹溺后肺损伤的重要介质,但可能参与淹溺后期的肿损伤作用。

The pathophysiology of pulmonary damage in secondary drowning is not clear.Some authors thought that not only anoxia and hypo-osmolality,but also other mediators were involved in pulmonary damage in fresh water drowning.The purpose of this study was to observe the course of pathology,and to evaluate the role played by TNF,TXB_2,ACE in the pathogenesis of pulmonary damage in near drowning. Model:Carlen's tube was inserted endotracheally to isolate left from right bronchus of dog.Fresh water was poured into fight lung to simulate the process of drowning. Results:①In the fight lung,after 15 minutes of drowning appeared distenttion of the alveoli,and scattered rupturing of alveolar walls.By 3 hours,dogs were in severe respiratory distress state with bloody edematous fluid outpouring from right lung;6 hours after drowning,right lung appeared severe edematous and hemorrhagic,alveolar-capillary membrace was damaged;②In the left lung,after one hour of drowning,the type Ⅰ alveolar cells were slightly swollen,no change was observed in the type Ⅱ alveolar cells.A few endothelial cells were slightly swollen ;By three hours of drowning,some type Ⅱ epithelial celis began to proliferate,6 hours after drowning both epithelial and endothelial were severe swollen or disrupted,but alveolar-capillary membranes were intact;③drowning dog rapidly deteriorated gas exchange,and appeared severe hypoxia;④Serum ACE decreased from 35.53±4.7 u/ml(prot) to 18.11±7.211 u/ml (P<0.01 ) at six hours of drownin;⑤plasma TXB_2 rose from 128.27±40.586 pg/ml(prot) to 944.981 ± 273.418 pg/ml(P<0.01) at one hour after drowning and mantained at high levels throughout experiment;⑥Plasma TNF were 1.23±1.0 ng/ml (P< 0.05),no statistical significance.At six hour of drowning,plasma TNF significantly rose to 4.03± 2.6ng/ml(P<0.05);⑦After 15 minutes of drowning,surfactant of right lung was 1.59±0.85 mg/g and left lung was 4.46±0.94 mg/g (P<0.01);By 6 hours of drowrling surfactant of fight lung was C.95±0.11 mg/g,and lift lung was 1.77±0.99mg/g(P<0.01). Summary:We concluded that both direct and indirect damage of near drowning could result in pulmonary damage;The pathogenesis of projectile pulmonary edama was that alveolar capillary membranees were severe damaged.Time sequence studies in near drowning showed progressive cellular damage,with the type Ⅰ pulmonary epithelial cells demonstrating alteration earlier than the type cells; Both TXB_2 and ACE were involved in pulmonary damage of drowning.But they were not the marker of pulmonary damage of drowning;TNF was not an important mediator of pulmonary damage of drowning,but it was involed in pulmorary damage in later phase of drowning.