Objective To investigate the changes and roles of myocardial adenosine triphosphate enzyme(ATPase) in the mechanism of cardiac dysfunction after blunt chest trauma（BCT）. Methods Thirtysix rabbits were divided into 6 groups with random number table, control group, 2 h group, 4 h group, 8 h group, 12 h group and 24 h group, 6 in each group. The models of BCT were established with BIMⅡ biological impact machine, catheterization technique was used through the right jugular artery into the left ventricle measure its pressure. The hemodynamics and the activities of ATPase in myocardial cell plasm, homogenate and mitochondria were measured at preinjury(control group), 2 h, 4 h, 8 h, 12 h and 24 h postinjury. Results Left ventricular endsystolic pressure(LVESP), the maximal ascending rate of left intraventricular pressure(+dp/dtmax), isovolemec pressure(IP) and the maximal physiological velocity(Vpm) decreased significantly at 2 h group after BCT(Plt;0.05）, and recovered to preinjury level in 4 h, 8 h and 12 h group during 4-12 h after BCT; isovolumic relaxation phase left ventricular pressure descending time constant (T). Left ventricular enddiastolic pressure(LVEDP) and the maximal descending rate of left intraventricular pressure(-dp/dtmax) were significantly higher （Plt;0.05, 0.01）. The activity of ATPase in homogenate, mitochondria and cell plasm decreased significantly at 2 h group and 4 h group after BCT（Plt;0.05, 001, respectively）, and 8 h group and 12 h group recovered after BCT. There was negative correlations between [CM(159mm]LVEDP and -dp/dtmax and the decrease of the activity of Na+-K+-ATPase in homogenate（r=-0.674, -0.691, Plt;0.05）, the Ca2+-ATPase in homogenate（r=-0.613,-0.642, Plt;0.05）, the Na+-K+-ATPase in mitochondria（r=-0.622,-0.616, Plt;0.05）,the Ca2+-ATPase in myocardial cell plasm（r=-0.672,-0.658, Plt;0.05）, the Na+-K+-ATPase in myocardial cell plasm（r=-0.627,-0.632,Plt;0.05）,and the Mg2+-ATPase in myocardial cell plasm（r=-0.677,-0.661, Plt;0.05）. Conclusion The left ventricular function is impaired obviously after BCT, especially in diastolic phase. The decrease of the activity of ATPase in myocardial cells may be one of the reasons of cardiac dysfunction after BCT.
Objective To investigate the changed rules of the cardiac functions in rabbits and to provide theoretical gists for clinical diagnosis and treatment after blunt chest trauma(BCT). Methods Using the models of moderate to severe BCT with BIM-Ⅱ Bio-impactor in 20 rabbits to examinate the cardiac functions with cardiac catheterization, the single photonemission computed tomography(SPECT) and the Doppler echocardiography at preinjury and 1h, 2h, 4h, 6h, 8h, 12h and 24h after BCT. Results Central venous pressure( CVP）, left ventricular enddiastolic pressure (LVEDP) and the decreasing time constant of left intraventricular pressure (T) at 24h after trauma were higher obviously than those before trauma (Plt;0.05,0.01). The -dp/dtmax at 24h after trauma was lower markedly than that before trauma (Plt;0.05 ). The ejection fraction(EF),1/3 EF, 1/3 ejection rate（1/3ER） and the ratio of 1/3 filling rate (1/3FR) to 1/3ER of the right ventricle at 24h after impacted were lower markedly than those before impacted (Plt;0.05). The peak filling rate, 1/3 filling fraction, 1/3 filling rate, the ratio of peak filling rate to peak ejection rate and the ratio of 1/3FR to 1/3ER of the left ventricular at 24h after impacted were lower obviously than those before impacted (Plt;0.05, 0.01). Conclusion The cardiac functions are changed significantly after BCT. The expressions of the right ventricular dysfunctions mainly are systolic dysfunction while the left ventricular dysfunctions are mainly diastolic dysfunction after BCT. All the cardiac catheterization, SPECT and the Doppler echocardiography are beneficial to the diagnosis of cardiac dysfunction after BCT. The SPECT is more exactitude and the Doppler echocardiography is more cheaper.