| Objective This paper aims to observe the effects of whole-body hypothermia on water content and pathological changes in the lungs of rats with smoke inhalation injury and to examine whether whole-body hypothermia can inhibit excessive systemic inflammatory response caused by smoke inhalation injury.Methods 54 healthy male SD rats (200~220g) were divided into 3 groups at random with 18 in each group: the normal control group, the pure inhalation injury group and the whole-body hypothermia group. Give the rats a fast of 12hrs prior to experiment with free access to water and the ambient temperature being (23~25)℃. After peritoneal injection of pentobarbital natrium (40mg/kg) of 2% concentration, the rats were anaesthetized. Then the rat models of smoke inhalation injury were made according to specific references. 30min after modeling the normal control group and the pure smoke inhalation injury group were put in a thermostat water bathtub to maintain their rectal temperature (38±0.5)℃, with the indoor temperature being (25~27)℃. Spray alcohol on the surface of the rats in the whole-body hypothermia group to lower their rectal temperature to (33±0.5)℃. When their rectal temperature reached the specified point it was maintained for 1h. 10~15min after hypothermia treatment the rectal temperature was raised to normal temperature which was then maintained until the end of the experiment. 2ml of blood of abdominal aorta was collected from each rat in the 3 groups at 6h after smoke inhalation injury and was centrifuged to obtain serum albumin in which the contents of tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) were measured. The left lungs was excised for measurement of water content in lungs and the right lower lungs was excised and fixed by formaldehyde solution of 4% concentration to make pathological sections.Results The wet-to-dry weight ratios of lung tissues in the normal control group, the pure smoke inhalation injury group and whole-body hypothermia group were 4.72±0.23, 6.53±0.62 and 5.40±0.47 respectively. It can be seen that the wet-to-dry weight ratios of lung tissues in the pure smoke inhalation injury group and the whole-body hypothermia group were significantly higher than that in the normal control group (P<0.05) and the wet-to-dry weight ratio of lung tissues in the whole-body hypothermia was lower than that in the pure smoke inhalation injury group (P<0.05). Under optical microscope it can be seen that the alveoli of rats in the normal control group were morphologically normal and structurally integral, the alveolar wall was smooth, alveolar septum was even and there was no exudate or leucocytes in the alveolar space, while in the pure smoke inhalation injury group the structure of the alveolar of rats was disrupted, alveolar wall became thicker with apparent congestion, and infiltration of inflammatory cells and fluid exudation can be seen in alveolar walls, pulmonary interstitial and alveolar space. After being treated with whole-body hypothermia the structure of alveolar of rats became much clear, and the alveolar wall thickening and inflammatory cell infiltration were lessened. The content of TNF-αin the normal control group was 26.7±3.1(pg/ml), and that in the pure smoke inhalation injury group and the whole-body hypothermia group were 108.6±10.5 and 73.8±11.6 (pg/ml) respectively. The respective contents of IL-6 were 58.4±5.3, 162.1±12.7 and 125.3±13.1(pg/ml) in the normal control group, the pure smoke inhalation injury group and the whole-body hypothermia group. The contents of IL-6 and TNF-αboth in the pure smoke inhalation injury group and the whole-body hypothermia group were notably higher than that in the normal control group (P<0.05), and when compared with the pure smoke inhalation injury group the contents of IL-6 and TNF-αwere remarkably lower (P<0.05)in the whole-body hypothermia group.Conclusions 1. After smoke inhalation injury the water content increased and severe pathological changes appeared in the lungs of the rats, and the contents of pro-inflammatory mediators TNF-αand IL-6 increased in the blood circulation. 2. When treated with hypothermia 33℃the water content was decreased and the inflammatory cell infiltration was reduced in the lungs of the rats with smoke inhalation injury. 3. 33℃hypothermia treatment can also inhibit the increase of systemic inflammatory mediators caused by smoke inhalation injury. 4. No influence was observed of 33℃hypothermia treatment on rat's blood clotting in this experiment. |
PDF Full Text Request