沙漠干热环境下中暑大鼠的心肌酶及心肌组织形态学改变

Changes of myocardial enzymes,histology and ultrastructure of heat stroke rats in dry-heat desert environment

目的探讨沙漠干热环境下中暑对大鼠心肌损伤的影响。方法 48只雄性SD大鼠随机平均分成6组:沙漠干热环境轻度中暑组及其常温对照组,中度中暑组及其常温对照组,重度中暑组及其常温对照组,然后将3个实验组大鼠分别置于干热环境(温度:41℃,湿度:10%),3个对照组大鼠置于常温环境(温度:25℃,湿度35%)中,在建立沙漠干热环境中暑大鼠后,干热环境组及其对照组分别在实验开始70 min(轻度中暑)、110 min(中度中暑)、145 min(重度中暑)被处死并取材。用全自动生化检测仪检测大鼠血清心肌酶CK(磷酸肌酸激酶)、CK-MB(肌酸激酶同工酶)、LDH(乳酸脱氢酶)的变化,用HE染色观察心肌病理学变化,用电子显微镜观察心肌超微结构变化。结果干热中暑各组大鼠血清心肌酶CK、CK-MB、LDH较常温对照各组显著升高(P<0.05),干热组CK、CK-MB、LDH均随中暑程度加重而升高,其中CK和LDH的轻度中暑组与中度中暑或重度中暑组比较差异具有显著性(P<0.05),但中度中暑组与重中暑度组比较差异无显著性(P>0.05);干热中暑组CK-MB各个组间比较差异均有显著性(P<0.05);HE染色结果提示:干热中暑组心肌组织早期即心肌间血管明显出现扩张充血、出血,随热暴露时间延长充血、出血现象逐渐加重,常温对照组未见异常。电子显微镜结果显示:干热环境组心肌细胞部分肌丝紊乱断裂、溶解,Z线模糊消失,线粒体肿胀,线粒体基膜不清晰,见空泡形成,部分毛细血管内皮细胞增生,并随热暴露时间延长,心肌细胞损伤逐渐加重。结论沙漠干热环境可造成大鼠心肌损伤,并随热暴露时间的延长及中暑程度的加重而损伤逐渐加重。提示沙漠干热环境下中暑的治疗应注意加强心肌损伤的保护。

Objective To explore the myocardial enzyme, histology and uhrastructure changes of heat stroke rats in dry-heat desert environment. Methods Forty-eight male SD rats were randomly divided into 6 groups： mild heat stroke group and its control group, moderate heat stroke group and its control group, severe heat stroke group and its control group. Then the three experimental groups of rats were put into dry-heat environment （temperature 41℃ , humidity 10% ） and the three control groups were put into normal environment （temperature 25℃ , humidity 35% ）. After establishment of the heat stroke rat models, the rats were sacrificed at their corresponding time points （70, 110 and 145 rain） from the beginning of the experiment for the mild heat stroke group and its control group, moderate heat stroke group and its control group, and severe heat stroke group and its control group, respectively. Blood samples were taken and heart tissues were harvested. The serum enzymes CK, CK-MB, and LDH were detected by an automatic biochemical analyzer. The pathological examination was performed with HE staining and ultrastructural changes were observed by electron microscopy. Results The serum enzymes CK, CK-MB, LDH were significantly higher in the dry-heat stroke groups than that in their control groups （P 〈 0. 05）. The serum CK, CK-MB, LDH levels were increased along with the progression of heat stroke, of which, CK and LDH of the mild heat stroke group were significantly different compared with that of the moderate heat stroke group or severe heat stroke group （P 〈0.05）. However, there were no significant difference between the moderate and severe heat stroke groups （P 〉 0.05）. CK-MB levels were significantly different between every two groups of the three heat stroke groups （P 〈 0.05 ）. The pathological examination showed dilation and congestion of blood vessels and hemorrhage, which became more serious along with the prolongation of exposure to dry-heat. The control group showed no abnormalities. Electron microscopy showed disruption of myofilamcnts and myolysis, blurred Z lines, swollen mitochondria, cytoplasmic vacuolization in the cardiomyocytes of heat stroke rats, and all these myocardial cell injuries became more serious along with the progression of heat-stroke. Conclusions Dry-heat desert environment can cause myocardial injury, and gradually getting worse along with the prolongation of dry-heat exposure and progression of heat stroke. Our findings suggest that attention should be paid to protection of the myocardium against injurious effect of heat stroke in dry-heat desert environment.