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目的 建立长时程海水浸泡体温过低症SD大鼠模型,并对重要脏器病理损伤和血液学指标进行横断面观察.方法 成年雄性SD大鼠20只,按数字表法随机均分为正常对照组和低温实验组,每组10只.正常对照组不做处理,低温实验组20℃人工海水中浸泡24 h,观察低温海水浸泡过程大鼠生命体征变化,实验结束后检测各部位体温,常见血液学指标及重要脏器病理学改变.结果 低温实验组大鼠低温海水浸泡过程中,生命体征逐渐下降[心率:浸泡前(369.0±25.1)次/min vs浸泡后(126.5±8.6)次/min,P<0.05;呼吸频率:浸泡前(92.8±7.2)次/min vs浸泡后(43.9±3.8)次/min,P<0.05;肛温:浸泡前(37.3±0.3)℃vs浸泡后(21.9±0.8)℃,P<0.05].浸泡结束后,血液常规[血红蛋白:正常对照组(145.4±11.5)g/L vs低温实验组(129.5±12.1)g/L,P<0.05;中性粒细胞百分比:正常对照组(18.3±3.5)％vs低温实验组(34.9±6.1)％,P<0.05)、凝血功能(凝血酶原时间:正常对照组(11.42±2.36)s vs低温实验组组(17.86±2.41)s,P<0.05;活化部分凝血活酶时间:正常对照组(12.97±2.41)s vs低温实验组(17.28±2.33)s,P<0.05]、生化指标[谷丙转氨酶:正常对照组(70.40±15.48)U/L vs低温实验组(183±61.62)U/L,P<0.05;谷草转氨酶:正常对照组(115.1±14.8)U/L vs低温实验组(722.3±248.2)U/L,P<0.05;尿素氮:正常对照组(9.08±2.44)mmol/L vs低温实验组(21.45±3.43)mmol/L,P<0.05;肌酐:正常对照组(24.71±6.27)μmol/L vs低温实验组(28.08±5.19)μmol/L,P<0.05;CK-MB:正常对照组(451.00±266.53)U/L vs低温实验组(2854.4±1089.56)U/L,P<0.05].病理学提示重要脏器均出现不同程度损伤,肺脏和胃病理损伤最为严重,可见低温性胸水.结论 长时程海水浸泡体温过低症SD大鼠模型建立成功,肺脏和胃为重要的损伤靶器官,可用于后续相关研究.

Objective To establish hypothermia SD rat model induced by prolonged seawater immersion and to observe pathological damage to vital organs as well as certain important hematological parameters .Methods Twenty male adult Sprague-Dawley rats were randomly and equally divided into the normal control group and the hypothermia experimental group ( or simply the hypothermia group ) , each consisting of 10 rats.The control group was left there without any treatment , while the hypothermia group was immersed in artificial seawater at 20 ℃ for 24 hours to observe changes in vital signs of the rats during cold seawater immersion .At the end of the experiment , body temperature , general hematological parameters and pathological changes of vital organs were detected for further study .Results During the course of cold seawater immersion, the vital signs of the rats in the hypothermia group gradually worsened [( Heart rate before immersion (369 ±25.1) beats/min] vs (126.5 ±8.6) beats/min after immersion] (P<0.05).Respiratory rate before immersion was (92.8 ±7.2) times/min vs (43.9 ±3.8) times/min after immersion (P<0.05). Rectal temperature before immersion was (37.3 ±0.3) ℃vs (21.9 ±0.8) ℃ after immersion (P<0.05). After immersion, the blood routine detection indicated that hemoglobin level of the normal control group was (145.4 ±11.5) g/L, while that of the hypothermia group was (129.5 ±12.1) g/L ( P<0.05); neutrophil percentage of the normal control group was (18.3 ±3.5) ％, while that of the hypothermia group was (34.9 ± 6.1) ％(P<0.05).Prothrombin time (PT) of the normal control group was (11.42 ±2.36) s, while that of the hypothermia group was (17.86 ±2.41) s (P<0.05); APTT of the normal control group was (12.97 ± 2.41) s while that of the hypothermia group was (17.28 ±2.33) s (P <0.05).As for biochemical parameters, alanine aminotransferase (ALT) of the normal control group was (70.40 ±15.48) U/L, while that of the hypothermia group was (183.00 ±61.62) U/L (P<0.05); aspartate transaminase (AST) of the normal control group was (115.1 ±14.8) U/L, while that of the hypothermia group was (722.3 ±248.2) U/L (P<0.05);blood urea nitrogen (BUN) of the normal control group was (9.08 ±2.44) mmol/L, while that of the hypothermia group was (21.45 ±3.43) mmol/L (P<0.05);creatinine of the normal control group was (24.71 ±6.27) μmol/L, while that of the hypothermia group was (28.08 ±5.19) μmol/L (P<0.05);CK-MB of the normal control group was (451.00 ±266.53) U/L, while that of the hypothermia group was (2854.4 ±1089.6) U/L, with significant differences (P<0.05).Pathological detection indicated that there were lesions to various extents in all the vital organs , with the lesions to the lungs and stomach being most serious, and pleural effusion induced by hypothermia was also present .Conclusion The SD rat model of hypothermia induced by prolonged seawater immersion was successfully established for subsequent studies .Our present study showed that lungs and stomach were important target organs involved in prolonged seawater immersion.