| Objective: This study took use of the direct method of burns caused by hot water to build the rat model, to observe the early situation of myocardial damage in rats, to explore the protective effect of enalaprilat’s early intervention in myocardial damage in severely burned rats and to preliminarily study its mechanism of action.Methods: 66 SD rats, female, these experimental animals were randomly divided into normal control group, burn group and treatment group.(1) Normal control group with 6 rats: weigh after anesthesia; take Blood samples from the abdominal aorta for correlation detection; the animals were put to death, and cardiac tissues were taken to do relative testing.(2) Burned animals: weigh after anesthesia; after scalding verdict compound Ringer solution(according to the parkland formula, 4.0ml / kg / TBSA%) intraperitoneal injection of anti-shock fluid. Take abdominal aortic blood respectively, in a total of five time points, i.e. 1,3,6,12,24 h after injury, and kept heart tissue specimens. Use the enzyme-linked immunosorbent assay(ELISA) to detect Serum Ang II, c Tn I, IL-1, TNF-α levels, cardiac Ang II, SOD, MDA, Na +, K +-ATP enzyme, Ca2+-ATP enzyme levels. Part of myocardial tissue applied DNA terminal transferase-mediated nick end labeling(TUNEL) method to detect apoptosis, SP method to detect the expression of Bcl-2, Bax; at each time point took six rats.(3) treatment group: weigh after injection of anesthesia; After the verdict, inject compound forest burns liquid(as parkland formula, 4.0ml / kg / TBSA%) by intraperitoneal injection of fluids to anti-shock; as for the enalaprilat group, fill in anti-shock liquid by 1mg / Kg and do the same procedure with the second group after 1, 3, 6, 12,24 h of injury respectively; each time point take six rats.(4) Use SPSS 16.0 statistical software for data analysis, all data are stated in the form of "mean ± standard deviation”.The result:1.Variation of the levels of c Tn I, IL-1, TNF-α in the Serum.Levels of c Tn I, IL-1, TNF-a in the serum of burned rats at each time point after injury significantly increased(P <0.05), the serum c Tn I, IL-1, TNF-α levels of both groups after injury first increased, peaked at 3h,(651.91 ± 22.57)pg / ml and(520.69 ± 25.04)pg / ml,(501.7 ± 10.01)pg / ml and(382.65 ± 15.60)pg / ml),(422.95 ± 10.90) pg / ml and(356.32±18.01)pg / ml; after that showed a downward trend. Compared with burn group, the levels of c Tn I, IL-1, TNF-α in the serum of the treatment group decreased(P <0.05).2.Variation of the activity of SOD,MDA,Ca2 +-ATPase and Na +,K +-ATPase in rat’s myocardial homogenates.The myocardial SOD’s activity of burned rats at 3, 6, 12, 24 h after injury significantly decreased(P <0.05). Both group decreased progressively after injury, reaching the end value at 12 h,(33.64± 6.52)U / ml and(36.46 ± 1.85)U / ml, after that rose; Content of myocardial MDA at 3, 6, 12, 24 h after burning significantly increased(P <0. 05); the content of the two groups began to increase after injury, peaked at 12 hours(5.66 ± 0.21)mmol / ml and(4.89 ± 0.15) mmol / ml, after that showed a downward trend.while the activity of Ca2 +-ATPase at 3, 6, 12 and 24 h after injury significantly decreased(P <0.05), both group decreased progressively after injury, reaching the end value at 12 h,(1.54 ± 0.20)ng / ml and(1.81 ± 0.19)ng / ml, after that came to rising; Activity of Na+,K+- ATPase decreased significantly in 6,12,24h(P <0.05), both group decreased progressively after injury, reaching the end value at 12 h,(1.49±0.23)ng/ml and(2.11±0.12)ng/ml, after that increased. Compared with burn group,the activity of SOD、Ca2+-ATPase and Na+,K+-ATPase in myocardial homogenate increased much more in to varied degrees.(P <0.05).the MDA content was decrease.(P <0.05)3. Variation of the content of rat’s serum and myocardial homogenates Ang II.myocardial homogenates and serum Ang II of burn group at 1,3, 6, 12, and 24 h after injury showed a significant increase(P <0.05), both of the two groups first raised afterinjury, peaked at 3h, i.e.(2.74 ± 1.15)ng / ml and(2.16 ± 0.31)ng / ml and(461.69 ± 46.19)pg / ml and(409.55 ± 16.60)pg / ml; after that declined. serum and myocardial homogenates Ang II levels was significantly higher than those of the burn group(P <0.05). Contents of rat’s serum, myocardial homogenates Ang II of the group with Enalaprilat treatment decreased significantly compared with that of the burn group.4.Rats myocardial apoptosis and the expression of Bcl-2 and Bax.The number of apoptotic cells significantly increased after burning at all time points, and gradually increased and peaked at 24 h. Compared with the burn group, number of apoptotic cells of the treatment group significantly reduced at each time point; Bcl-2 expression gradually decreased, up to the lowest value at 12 h. Compared with the burn group, the expression of treatment group significantly increased at 3, 6, 12, 24 h(P <0.05); the expression of Bax significantly increased at all time points, first rose and peaked at 12 h and then showed a decline trend; the ratio of Bcl-2 / Bax’s first declined, reaching the lowest value at 12 h, and then rose; it is negatively correlated with the number of apoptotic cells(r=-0.763,P=0.006).Conclusion: Severely burned rats got myocardial injury very early, accompanied by a large number of inflammatory mediator release, lipid peroxidation,Lower levels of proton pump and apoptosis, and Ang II massive release; while the use of enalaprilat on rats can reduce myocardial injury, this may be because that enalaprilat can reduce the release of Ang II after burns, thus causing the reduction of the generation and release of inflammatory media, elevated levels of proton pump, the enhancement of antioxidant capacity, as well as the reduction of myocardial apoptosis pathway so to achieve the protective effect on myocardium. |
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