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.
OBJECTIVE: To explore the molecular mechanisms involved in the increased collagen synthesis by platelet-derived wound healing factors (PDWHF) during wound healing in alloxan-induced diabetic rats. METHODS: Thirty-three male SD rats were divided into two groups, the normal (n = 9) (group A) and the diabetic group (n = 24). Two pieces of full-thickness skin with diameter of 1.8 cm were removed from the dorsal site of diabetic rats. PDWHF (100 micrograms/wound) was topically applied to one side of the diabetic wounds (group B) on the operation day and then once a day in the next successive 6 days. Meanwhile, bovine serum albumin (100 micrograms/wound) was applied to the other side of diabetic wound as control group (group C) in the same way. Levels of transforming growth factor-beta 1 (TGF-beta 1) and procollagen I mRNA in wound tissue were inspected by dot blotting. RESULTS: TGF-beta 1 mRNA levels in group B were 4 folds and 5.6 folds compared with those in group C after 5 and 7 days (P lt; 0.01), however, still significantly lower than those of group A (P lt; 0.05). There was no significance difference among three groups on the 10th day after wounding. The levels for procollagen I mRNA in group B amounted to 2.1, 1.8 and 2.3 folds of those in group C after 5, 7, and 10 days (P lt; 0.01), respectively. Compared with those in the group A, procollagen I mRNA levels in the group B were significantly lower after 5 and 7 days (P lt; 0.05), and no significant difference was observed between group B and A after 10 days. CONCLUSION: One important way for PDWHF to enhance the collagen synthesis in diabetic wound healing is to increase the gene expression of endogenous TGF-beta 1.
OBJECTIVE: To describe the concept of "un-controlled wound repair" and review its current progress in basic research and clinical treatment. METHODS: The literature review and comprehensive analysis methods were used in this study. RESULTS: The results showed that the normal wound repair and "un-controlled" wound repair had made big progress in cellular, molecular and genetic levels in recent years and these progresses had enhanced the treatment progress in clinic. CONCLUSION: All data indicate that the wound repair is made a big progress both in basic and clinic fields. New high techniques, such as clone, biochip and stem cell and their use will promote the deep study of "un-controlled" wound repair.