建立严重、危重与极危重3个层级重度蒸汽吸入性损伤兔模型。

随机将136只新西兰大白兔分为假伤组(n＝34)与致伤组(n＝102)。致伤组按蒸汽吸入致伤时间分为0.25、0.50、1.00 s组(均n＝34)，0.25、0.50、1.00 s组兔用自动控时调压烫伤仪^[11,12]控制蒸汽压力0.02 MPa/cm²、温度105 ℃条件下通过气管切开处分别致伤，假伤组兔除不予吸入蒸汽致伤外其它处理同致伤组。0.25、0.50、1.00 s组与假伤组于伤后1、4、12、24 h各取兔6只检测或观察动脉血氧分压(PaO₂)与二氧化碳分压(PaCO₂)、肺组织病理、肺组织含水率变化，各组另取10只兔观察伤后6、12、24 h死亡率。

1.00 s组伤后1 h即出现明显的肺充血水肿和出血、缺氧以及炎症细胞浸润状况并逐渐加重，伤后6 h兔死亡率达100%。0.50 s组伤后1 h也出现肺充血水肿和出血、缺氧，至伤后4 h加重并出现炎症细胞浸润，伤后1、4 h的PaO₂较1.00 s组高，差异有统计学意义(P<0.05)，0.50 s组兔伤后12、24 h死亡率分别为25%、75%。0.25 s组在伤后4 h出现肺充血水肿、缺氧，伤后12 h肺充血水肿加重并出现出血、炎症细胞浸润，伤后4、12、24 h PaO₂均小于60 mmHg(1 mmHg＝0.133 kPa)，较0.50 s组同时相点高，差异有统计学意义(P<0.05)，较假伤组同时相点低，差异均有显著性统计学意义(P<0.01)，0.25 s组伤后24 h兔死亡率为25%。

在蒸汽压力为0.02 MPa/cm²，温度105 ℃条件下，致伤时间1.00、0.50、0.25 s可分别造成兔极危重、危重和严重吸入性损伤。

To establish serious, critical and extra-critical model of severe inhalation injury induced by steam in rabbits.

One hundred and thirty six New Zealand white rabbits were randomly divided into the injury groups with 102 rabbits and the sham group with 34 rabbits. According to the injury time the injury groups were randomly divided into 3 groups and each group included 34 rabbits and those groups were respectively named the group of 0.25 s, 0.50 s, 1.00 s. After placed a 5-mm inside diameter tracheal tube, animals in the injury groups were vulnerated by steam that came from an "automatic control time and pressure scald instrument" made at our lab which ensured the steam pressure 0.02 Mp/cm² and temperature 105 ℃. In the injury groups the injury time was respectively 0.25 s, 0.50 s, 1.00 s. Except inhalation injury induced by steam, the same treatment was given to the sham group with 34 animals as the injury groups. Throughout the experiment, We measured PaO₂, PaCO₂ of arterial blood sample using an automatic blood gas system in each group with 6 rabbits at each post injury time point (1 h, 4 h, 12 h, 24 h). we also examined the lung histopathology, the lung dry/wet weight ratio in each group with 6 rabbits at each post injury time point (1 h, 4 h, 12 h, 24 h). We recorded the mortality rate in each group with additional 10 rabbits at various post injury time point (6 h, 12 h, 24 h).

At 1 h of post injury the group of 1.00 s appeared the changes that included significant pulmonary congestion, edema , bleeding, hypoxia and inflammatory cells infiltration. The above changes were gradually aggravated with time and the mortality of rabbits at 6 h of post injury was 100%. At 1 h of post injury the group of 0.50 s also appeared the changes that included pulmonary congestion, edema, bleeding, hypoxia. The above changes were gradually aggravated at 4 h of post injury and inflammatory cells infiltrated into the lung tissue. PaO₂ in the group of 0.50 s was higher than the group of 1.00 s at 1 h, 4 h of post injury, which indicated a statistical significance (P<0.05). The mortality of rabbits of the group of 0.50 s at 12 h, 24 h of post injury was 25%, 75%. In the group of 0.25 s, pulmonary congestion, edema and hypoxia were observed at 4 h of post injury. At 12 h of post injury , pulmonary congestion and edema combined with pulmonary bleeding, hypoxia and inflammatory cells infiltration were gradually aggravated in the group of 0.25 s. PaO₂ in the group of 0.25 s decreased to a level of less than 60 mmHg at 4 h, 12 h, 24 h of postinjury. PaO₂ in the group of 0.25 s was higher than the group of 0.50 s at the same time-point of post injury, which indicated a statistical significance (P<0.05). PaO₂ in the group of 0.25 s was lower than the sham group at the same time-point of post injury (P<0.01). The mortality of rabbits of the group of 0.25 s at 24 h of postinjury was 25%.

By inhaling the steam of 0.25 s, 0.50 s, 1.00 s that the steam pressure was 0.02 Mp/cm² and temperature was 105 ℃, the stable serious, critical and extra-critical model of inhalation injury induced by steam can be reproduced in rabbits.