The Study Of Secondary Myocardium Injury Caused By Mechanical Trauma

Aim: This experiment is to establish models of mechanical trauma and observe thechanges of myocardial in models of mechanical trauma. Methods: SD rats were used toestablish animal models of mechanical trauma, they were divided randomly into fourgroups, control group and different trauma group,10rats each group. The trauma grouprats were anesthetized with pentobarbital sodium (40mg/kg), then were placed in ahomemade small animal quantitative trauma device individually. Those rats weretraumatized as the wheel rotated (100revolutions、200revolutions、400revolutions at arate of40r/min). After12hours, corresponding measures were taken to observe thepathological changes of myocardial finally, those indexes include the changes of theultrastructure of myocardial, the changes of apoptosis factors caspase-3, the changes ofthe fuction of myocardial, the intracellular concentration Ca2+. Results: Compared withthe control group,the function of the heart injuried, for example,the heart diastolicpressure decreased(P<0.01), the left ventricular pressure maximal rate of rise (+dp/dtmax) decreased (P<0.01), the left The maximum rate of ventricular pressure(-dp/dtmax) drop (P<0.01); the changes of the ultrastructure of myocardial obviousclear，for example, plastosome damaged, an increased of the number, morphologicalchanged； cell nucleus damaged, nucleolus burst and margination; blood capillaryinjuried and so on; apoptosis factor caspase-3activity increased (P<0.01), theintracellular concentratrion of Ca2+increased (P<0.01or<0.05), and the fuction ofmyocardial dysfunction in the trauma group. Conclusion: mechanical trauma cause thehurt of cardiac fuction and myocardial, and this hurt will be severed because of the increase of injury severity.