Background: Craniocerebral injury can cause a series of visceral complications, among which cardiovascular complication is paid special attention. Objective: To investigate the effects of craniocerebral inju ry on changes of circulatory and local angiotensin II (Ang II ) and local angiotensin II receptor 1 (AT1) in the heart. Design: Randomized contro lled experiment taking animals as subjects. Setting: Beijing Tiantan Hospital, and the College of Basic Medicine, Capital University of Medical Sciences. Materials: The experiment was c onducted at the Central Laboratory of Capital University of Medical Sciences and the Central Laboratory of Beijing Tiantan Hospital from 2003 to 2004. Totally 40 healthy male Wistar rats were divided randomly into craniocerebral injury group and control group with 20 in each group. Methods: Rats in craniocerebral in jury group were treated with weight-drop method to establish the model of craniocerebral injury, while rats in control group received no impact. Twenty-four hours after hitting, 10 rats in each group were selected to assay their Ang II and AT1; the other 10 in each group were selected, to observe their myocardial forms. Main outcome measures: 1 Level of plasma Ang II with competitive radioimmunoassay; 2 expression of Ang II and AT1 with immunohistochemistry; 3 activity of MB isoenzyme of creatine kinase (CK-MB) with enzyme reaction rate method; 4 pathomorphological changes of myocardium of rats assayed with light microscope after hematoxylin-eosin staining and transmission electron microscope. Results: Totally 40 rats entered the final analysis. 1 Level of Ang II: It was significantly higher in craniocerebral injury group than in control group [(965.52±176.71), (485.03±86.13) ng/L, P < 0.05]. 2 CK-MB activity: It was obviously higher in craniocerebral injury group than in control group [(12.77±4.07), (3.49±1.55) μkat/L, P < 0.05]. 3 Expression of Ang II and AT1: The area of positive reactant and gray value in craniocerebral injury group were higher than those in control group (P < 0.05). 4 Hematoxylin-eosin staining: Strong acidophil staining was found on myocardial cellular plasma in craniocerebral injury group. The results showed that cytoplasm shrank obviously; muscle fiber broke, decreased or disappeared. Focal hydropic degeneration, lysis or necrosis was observed in myocardium. Ultrastructural pathological observation revealed pathological damage of myocardium. Conclusion: Craniocerebral injury in rats can cause myocardial damage, and changes of angiotensin system may be one of the factors.