动物造模,急性肝损伤 z-bio 2022-06-29 836

　　Objective To investigate the effect of carbon tetrachloride (CCl4) on cardiac function and morphology in rats with acute liver injury.

　　Methods A rat model of acute liver injury was induced by intraperitoneal injection of low, medium and high concentrations of CCl4, while an equal volume of vegetable oil was intraperitoneally injected as a normal control group. The electrocardiogram was detected at 24 h and 48 h, and the animals were sacrificed after the abdominal aorta was collected; the serum alanine aminotransferase (ALT) and cardiac troponin I (cTn I) levels were determined by enzyme-linked immunosorbent assay. ; Liver and heart tissue were made into sections and stained with HE, and the pathological changes were observed by light microscope; the myocardial tissue malondialdehyde (MDA), superoxide dismutase (SOD) and creatine were measured by visible light spectrophotometer Kinase (creatine kinase, CK) content.

　　Results The changes of serum ALT content and liver morphology of the rats in the model group proved that the CCl4-induced acute liver injury model was successfully established, and the degree of liver injury was in a certain concentration-dependent manner with CCl4. ECG detection showed that the ECG of rats in the model group showed different degrees of electrophysiological changes such as the elevation of the ST segment dorsal arch, the high peak of the T wave, and the prolongation of the Q-T interval. HE staining showed that the cardiac tissue had obvious pathological changes, and the degree of myocardial cell inflammatory reaction, edema and necrosis gradually increased with the increase of CCl4 injection concentration. The level of serum cTnⅠ was significantly increased (P<0.01), the content of CK and MDA in myocardial tissue was significantly increased (P<0.05), and the content of SOD was significantly decreased (P<0.05). 48 h is more significant.

　　Conclusions The hearts of rats with acute liver injury induced by CCl4 also undergo functional and morphological changes, and the degree of myocardial injury is concentration- and time-dependent.