| PurposeTraumatic rat models were established using the Noble-Collip drum, to observe whether the vasodilation of rats’renal and coronary arteries changed after trauma. If changes occurred, then the possible mechanism and relationship between the changes in endothelial-dependence vasodilator function of renal and coronary arteries and delayed cardiac dysfunction induced mechanical trauma were explored.Method1. Animal and grouping1) Healthy male wistar rats were randomly divided into two groups:trauma group and pseudo-trauma group.2) The pseudo-trauma group and trauma group were randomly divided into four groups:according to Oh,6h,12h,24h after trauma.2. Preparation of mechanical trauma modelAccording to the experimental method of our preliminary studies, we established a mechanical trauma model in rats. The rats were anesthetized with sodium pentobarbital (0.04mg/g, i.p), placed into a Noble-Collip drum (diameter:30.5cm) and were subjected to200revolutions at a rate of40rpm. As the wheel was rotated, trauma rats were traumatized, while sham trauma rats were fixed to the drum with tape. The sham trauma rats only accompanied by the Noble-Collip drum rotation instead of falling from height.3. Mensuration of indicators1) Traumatic rat models were established using the Noble-Collip drum according to the experimental method of our preliminary studies. Cardiac function in vitro was assessed through a Langendorff heart perfusion apparatus.2) In order to investigate the reason of delayed cardiac dysfunction induced by mechanical trauma, Danish Myo Technology (DMT) was used to detect the diastolic function of isolated renal and coronary arteries in traumatized rats.3) To explore the possible mechanism of change in endothelial-dependence vasodilator function of coronary arteries. We tested the contents of Ang Ⅱ in the rat serum and myocardial tissue by ELISA and analyzed the relationship between Ang Ⅱ in serum and myocardial tissue and cardiac dysfunction induced by mechanical trauma. 4. Statistical analysisAll calculations and statistical analyses were performed using the statistical software program SPSS17.0. All values are presented as means±SEM. Differences between two means were compared by Student’s t test. All of the other values were analyzed by ANOVA followed by a Fisher least significant difference (post hoc) test for multiple comparisons, Multi-way ANOVA was used to compare between the two groups at different time points. Logistic curve fitting on results of isolated arterial rings was analyzed by GraphPad Prism4.0. The Ang Ⅱ relationship uses correlation analysis between the serum and cardiac tissue, the Ang Ⅱ in serum and myocardial tissue and cardiac function in vitro after trauma. Probabilities of P<0.05were considered statistically significant.Results1. The cardiac function of rats24h after trauma significantly decreasedCompared with the sham group, there was no obvious change in+dp/dtmax and-dp/dtmax in vitro within24h after mechanical trauma. However, the cardiac function of rats24h after trauma significantly decreased.[+dp/dtmax:(5506±179.7)mmHg/sec vs.(3455±310.6)mmHg/sec, P<0.01;-dp/dtmax:(-3433±335.7)mmHg/sec vs.(-5205±171.0)mmHg/sec, P<0.01].2. The maximum endothelium-dependent relaxation of isolated coronary rings obviously decreased24h after trauma, but not6h after traumaOnce a stable contraction was achieved, the rings were exposed to cumulative concentrations of endothelium-dependent vasodilator (10-8-10-5mol/L, BK). The maximum endothelium-dependent relaxation of isolated coronary rings was obviously decreased24h after trauma, but not6h after trauma [Sham vs.6h after trauma:(39.57%±6.14%)vs.(35.57±%±7.30%), P>0.05; Sham vs.24h after trauma(39.57%±6.14%),(35.57±%±7.30%)vs.(24.08%±6.25%), P<0.05],The relaxation of rats’coronary artery rings on BK dose-response curve was significantly shifted to the right24h after trauma. When given the cumulative concentration (10-10-10-6mol/L), the vasodilatation of coronary artery rings24h after trauma response to SNP is no significant change compared to the sham group.3. The maximum endothelium-dependent relaxation of isolated renal artery rings obviously decreased6h after trauma.Once a stable contraction was achieved, the rings were exposed to cumulative concentrations of endothelium-dependent vasodilator (10-8-10-5mol/L, Ach). The maximum endothelium-dependent relaxation of isolated renal artery rings obviously decreased6h after trauma [(29.39%±5.50%)vs.(53.59%±5.95%), P<0.01], When given the cumulative concentration (10-10-10-6mol/L), the vasodilatation of renal artery rings24h after trauma response to SNP is no significant change compared to the sham group. 4. The contents of AngⅡ in rat serum and myocardial tissue6,12,24h after trauma were higher than the sham groupCompared with the sham group, the Ang Ⅱ concentration of rat myocardial tissue and serum6,12,24h after mechanical trauma significantly increased [6h:(207.7±17.92)vs.(171.9±13.80)ng/ml,P<0.05;12h:(223.7±11.22) vs.(171.9±13.80) ng/ml,24h:(258.1±59.66)vs.(171.9±13.80)ng/ml,P<0.01] and [6h:(44.92±4.21)vs.(37.14±2.34)ng/ml, P<0.05;12h:(47.11±2.31)vs.(37.14±2.34)ng/ml,P<0.05;24h:(49.30±7.05)vs.(37.14±2.34)ng/ml,P<0.01]。5. There was positive correlation between the levels of Ang Ⅱ in serum and myocardial tissue after traumaThere was a positive correlation between the levels of Ang Ⅱ in serum and myocardial tissue after trauma (r=0.865, P<0.01).6. The contents of Ang Ⅱ in serum were negatively correlated to the maximum endothelium-dependent relaxation of isolated coronary ringsThe contents of Ang Ⅱ in serum were negatively correlated to the maximum endothelium-dependent relaxation of isolated coronary rings(r=-0.802, P<0.01).7. The correlation between Ang Ⅱ in myocardium tissue and cardiac function24h after mechanical traumaThe contents of Ang Ⅱ in myocardial tissue were negatively correlated to+dp/dtmax (r0.782, P<0.05) and positively correlated to-dp/dtmax (r=0.718,P<0.05)24h after mechanical trauma.Conclusions1. The reason of delayed cardiac dysfunction induced by mechanical trauma is the result of the change of endothelium-dependent diastolic dysfunction of the coronary artery.2. Angiotensin Ⅱ levels increased in myocardial tissue and serum induced change of endothelium-dependent diastolic dysfunction of the coronary artery after mechanical trauma. Angiotensin Ⅱ levels in myocardial tissue and serum are closely related to cardiac dysfunction. RAS activation in circulation and myocardial tissue plays an important role in the change of endothelium-dependent diastolic dysfunction of the coronary artery. |
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