论文部分内容阅读
目的 建立低温海水淹溺濒临死亡动物模型 ,为开展相关研究奠定理论基础。方法 将大鼠置于 16℃～ 18℃低温海水中 ,自由游动 ,直至沉入水底 ;迅速取出动物 ,置室温下于不同时间 (1、5、15、30及 6 0min)观察生命指征 ,快速自左心室取血 1ml行血气分析 ,处死动物 ,取左肺计算干湿重比值 ,透射电镜观察右肺超微结构。结果 动物入海水后约 15min呼吸暂停 ;出海水后肛温、肺干湿重比值、呼吸频率和心率明显降低 ,1min组呼吸频率达最低点 (47± 7)次 /min ,心率 (70±14)次 /min ;5min组肛温降至最低点 (2 0 .2 5± 0 .5 2 )℃ ,上述指标除肺干湿重比值外均呈上升趋势 ,6 0min组呼吸频率达 (111± 2 6 )次 /min、心率达 (177± 2 8)次 /min ,接近正常对照组水平 ,差异无显著性 (P>0 .0 5 ) ,而肛温 (2 3.82± 0 .72 )℃和肺干湿重比值 (0 .0 8± 0 .0 3)仍未达正常对照组水平 ,差异有显著性 (P <0 .0 1)。血pH、动脉氧分压 (PaO2 )及血氧饱和度 (SaO2 )明显降低 ,5min组降至最低点 [6 .6 7±0 .11、(5 .91± 2 .98)kPa、43.30 %± 15 .0 3% ],随后呈上升趋势 ;6 0min组血PaO2 (11.81± 1.45 )kPa及SaO2 (88.6 3%± 14.39% )接近正常对照组水平 ,差异无显著性 (P >0 .0 5 ) ,而血pH(7.10± 0 .14)仍未达正?
Objective To establish a near-death animal model of low temperature seawater drowning, which lays a theoretical foundation for carrying out related research. Methods Rats were placed in low temperature seawater at 16 ℃ ~ 18 ℃, swimming freely until submerged. Animals were quickly removed and their vital signs were observed at different times (1, 5, 15, 30 and 60 min) at room temperature , Quickly from the left ventricular blood 1ml blood gas analysis, sacrificed animals, take the left lung dry weight ratio, transmission electron microscopy of the right lung ultrastructure. Results: The rectal temperature, the ratio of lung wet weight to dry weight, respiratory rate and heart rate were significantly decreased after the animals were exposed to the sea water for about 15 minutes. The lowest respiratory rate was 47 ± 7 times / min in 1 min group, and the heart rate was 70 ± 14 ) Min / min. The rectal temperature dropped to the lowest point (2.02 ± 0.52) ℃ in 5 min group, except for the ratio of lung wet weight and dry weight. The respiration rate in 60 min group reached (111 ± (P <0.05), while the rectal temperature (2 3.82 ± 0.72) ℃ was significantly higher than that of the control group (P <0.05), and the heart rate reached (177 ± 28) times / And lung wet weight ratio (0.08 ± 0.30) still did not reach the level of normal control group, the difference was significant (P <0.01). Blood pH, PaO2 and SaO2 decreased significantly, reaching the lowest point in 5 min group [6.67 ± 0.11, (5.91 ± 2.98) kPa, 43.30% ± 15 .0 3%], followed by an upward trend; blood PaO2 (11.81 ± 1.45) kPa and SaO2 (88.6 3% ± 14.39%) in 6 0min group were close to the normal control group, the difference was not significant 5), while the blood pH (7.10 ± 0.14) is still not up?