| Objective Acute craniocerebral injury (ACI) model was established in rats by free falling objects hitting skull (Feeney method). To investigate the changes of myocardial ATPase activity and plasma tumor necrosis factor-alpha (TNF-a) levels in rats with acute craniocerbral injury (ACI), for better understanding the mechanism of myocardial injury after acute craniocerebral injuryMethods Seventy-two male Sprague Dawley rats were randomly (random number) divided into three groups including the normal group (N group)、 sham group (SHAM group) and acute craniocerebral injury model group (ACI group), which were fed for ten days in guangxi medical university animal experiment center. The observation intervals were set at2h,6h,24h and72h after ACI (n=8, at each intreval).(1) To establish acute craniocerebral injury (ACI) model by used of the free falling objects hitting skull (Feeney method). And to march the neurological deficit scores from the rat consciousness, feel, sports, behavior and basic reflection.(2) To measure plasma levels of cardiac troponin I (cTnI) and TNF-a in SHAM group and ACI group in all observation intervals (2h,6h,24h and72h) by collecting three milliliters abdominal aorta blood. The normal group was collected the same dose of sample after one hour. Plasma levels of cTnI and TNF-a were determined by using enzyme-linked immunosorbent assay (ELISA) in order to discuss the acute cranincerbral injury and to study the inflammatory mechanism of cytokine TNF-a in the myocardial damage after ACI.(3)0.2-0.4g heart tissue were taken to prepare homogenate in the observation intervals. And the activities of myocardial Na+-K+-ATPase, Ca2+-ATPase were determined by colorimetric method in order to discuss the mechanism of myocardial ATPase inactivation in the myocardial damage after ACI.(4) HE dyed for myocardial tissue and the pathological change of myocardial (HE staining) were observed by light-microscopy.Results(1) Each observation intervals of ACI group rats gradually appeared nervous defect symptoms. Compared with the ACI group, the levels of neurological deficit scores were all higher than the N group and SHAM group. The N group and SHAM group had not any obvious signs of neurological deficit in the experimental observation period.(2) There were swelling, cortex injury and tissue ooze blood in rats brain after ACI. The water content of brain tissue was significantly increased in2h and it reached the peak at24h after ACI. And there was no edema in N group and SHAM group.(3) Compared with the N group and SHAM group, the level of plasma cTnI increased significantly (P<0.05). The plasma level of cTnI began to rise in2h and reached the peak at24h and it was still high in72h. Cardiac structure of ACI rats present pathological changes, vacuolar degeneration and necrosis with inflammatory cell infiltrates of myocardium under light-microscopy. And there was no change in N group and SHAM group.(4) Compared with the N group and SHAM group, the level of plasma TNF-a increased significantly (P<0.05). The plasma level of TNF-a began to rise in2h and reached the peak at24h and it was still high in72h. And there was no significant difference between N group and SHAM group.(5) Compared with the N group and SHAM group, the activities of Na+-K+-ATPase, Ca2+-ATPase decreased significantly (P<0.05). The activity of myocardial Na+-K+-ATPase began to decrease in2h and touch the bottom at6h and it was still low in24h and72h. But the activity of myocardial Ca2+-ATPase began to decrease in6h and touch the bottom at24h and then it was still low in72h. And there was no significant difference between N group and SHAM group.(6) There was a negative correlation between myocardial Na+-K+-ATPase, Ca2+-ATPase activity and plasma levels of cTnI (r=0.357, r=0.557, P<0.05) And There was a positive correlation between plasma levels of TNF-a and cTnI (r=0.920, P<0.05), and a negative correlation between TNF-a and myocardial ATPase activity (r=0.259, r=0.452, P<0.05).Conclusions(1)Acute craniocerebral injury (ACI) model was established in rats by free falling objects hitting skull (Feeney method). The neurological deficit scores, brain edema degree and general observation of brain were accorded with acute craniocerebral injury clinical manifestations in ACI group. All results indicated that the ACI model built successful. (2) The increased plasma levels of cTnI and the morphologic changes of myocardium indicated that myocardial injury occurred in early stage.(3) ACI can lead to myocardial injury, resulting in increase in plasma TNF-a and decrease in myocardial ATPase activity. Decreasing in myocardial ATPase and increasing in TNF-a may involve in the pathogenesis of myocardial injury after ACI... |
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