Observation on the pathological and hematological parameters of the rats with hypothermia induced by prolonged seawater immersion

Abstract

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 (2 854.4±1 089.6) 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. Key words: Seawater immersion; Hypothermia; Pathology; Hematology