| BackgroundWith the development of modern industry, construction and transportation et al, the morbidity of mechanical trauma has gradually increased. Nowadays trauma has become the primary cause of death under the age of 45 years old. Recently, as the gradually improved on-site emergency measures, the direct damage caused by trauma has been controlled efficiently. However, secondary organic failures, especially heart failure, have been becoming important life-threatening pathophysiological changes. Recent clinical studies indicated that a few of patients feel good in the episode of clinical monitor, generally within 24 hour after trauma, but then the secondary injury has been observed such as myocardial dysfunction and infarction after they left the hospital. These investigations suggested that there were indirect secondary dysfunctions of circulatory system after trauma, but whether the dysfunction derived from heart or vascular or both have not been identifiedObjectiveTo clarify the possible indicators related to post-traumatic secondary dysfunction. of circulatory system through observing the dynamic changes of the cardiac and vascular function 24h after trauma in non-lethal mechanical trauma model.Methods1. The establishment of non-lethal mechanical traumatic rat model Male healthy SD rats (2-3 months,80) were randomly divided into two groups:sham trauma group and trauma group.(1) Sham trauma group:healthy adult rats were randomly selected, anesthetized with 10% chloral hydrate (0.3ml/100g, intraperitoneal injection), and then fixed on the inner wall of Noble-Collip trauma instrument (diameter:30cm; 40rpm,5mins). The rats were rotated in the trauma instrument but not fell from the height.①0 hour after sham group (0h):n=8②3 hour after sham group (3h):n=8③6 hour after sham group (6h):n=8④12 hour after sham group (12h):n=8⑤24 hour after sham group (24h):n=8 (2) Trauma group:After anesthetized (the method was the same as the former), the healthy male adult rats were palced into the Noble-Collip trauma instrument (40rpm,5mins), in which the rats fell from the height in the process of rotation. Then mechanical injury was induced in rats. Trauma group was randomly divided into the following groups:①0 hour after trauma group (Oh):n=8②3 hour after trauma group (3h):n=8③6 hour after trauma group (6h):n=8④12 hour after trauma group (12h):n=8⑤24 hour after trauma group (24h):n=82. Left Ventricular Systolic Pressure (LVSP), Left Ventricular Diastolic Pressure (LVDP), Left Ventricular End-Diastolic Pressure (LVEDP), left ventricular pressure rise/fall rate of the greatest change (+dp/dtmax and-dp/dtmax) and other cardiac hemodynamics index were monitored by MS2000 biological signal recording system.3. Diastolic function of thoracic aorta in rats was detected by isolated vascular rings technology.4. Serum high sensitivity C-reactive protein (hs-CRP) and myeloperoxidase (MPO) were detected by ELISA assay.Results1. Establishment of non-lethal mechanical trauma modelForty rats were placed into the Noble-Collip trauma instrument (40rpm,5mins). Two rats died in sudden from brain injury and the other were lived without hemorrhagic shock. MABP of sham trauma group and trauma group rats were more than 75mmHg within 24h after trauma, and there was no significant difference between the two groups (P>0.05). Additionally, in trauma group the mechanical trauma did not cause direct heart damage (such as pericardial hemorrhage, cardiac contusion, etc) and the behavior, diet and other activities of rats returned to normal in 2-3 hours after they waking up. The 24h survival rate in trauma group was 100%.2. Dynamic changes of cardiac function in non-lethal mechanical trauma rats2.1 After trauma myocardial contractile function had not changed±dp/dtmax and LVSP reflect cardiac systolic function. The results showed that compared with the sham trauma group,±dp/dtmax and LVSP of post-trauma Oh,3h,6h,12h,24h were no significant difference (P> 0.05).(Fig. 1,2,3)2.2 Post-traumatic myocardial diastolic dysfunction at 3 hours after nonlethal mechanical trauma.LVDP represents the left ventricular diastolic pressure, and LVEDP represents the left ventricular end-diastolic pressure. They can reflect cardiac diastolic function.The results showed that there was cardiac diastolic dysfunction after non-lethal mechanical trauma. Compared with the sham trauma group (LVDP:1.04±0.26mmHg. LVEDP:6.90±0.73 mmHg), LVDP (6.90±0.27 mmHg, P＜0.01) and LVEDP increased (27.02±2.03 mmHg,p＜0.01) in 3 hour after trauma group, but both LVDP and LVEDP recovered after 24 hours. (Fig.4,5)3. Post-traumatic endothelial diastolic dysfunction in nonlethal mechanical trauma ratsThe diastolic function of thoracic aorta was detected by isolated vascular rings technology. The results indicated that endothelium-dependent vasodilation significantly decreased 6 hour after trauma. Compared with the sham trauma.group (97.88%±9.52%), the maximum relaxation decreased significantly (50.50%±2.44%, P＜0.01), (Fig.6a,6b,7a,7b,8a,8b)4. Dynamic changes of hs-CRP and MPO after non-lethal mechanical trauma.4.1 Serum hs-CRP significantly increased after non-lethal mechanical trauma.High sensitivity C-reactive protein levels are the sensitive indicators of evaluating tissue damage. It not only can reflect the inflammatory activity but be considered to an important indicator of cardiovascular disease monitoring and prognosis judgment. We detect the hs-CRP in the non-lethal mechanical trauma rat model.The results showed that compared with the sham trauma group (4312.97±169.99ng/ml), serum high sensitivity C-reactive protein increased 24 hour after trauma (8306.22±425.64ng ml, P＜0.01) (Fig.9).4.2 Serum myeloperoxidase (MPO) levels did not change after mechanical nonlethal traumaMyeloperoxidase can be used as a predictor of cardiovascular events. The increase of the serum MPO levels reflect high incidence of cardiovascular diseases. Compared with the sham trauma group, there was no significant diffifence of serum MPO in the post-trauma Oh,3h,6h,12h, and 24h group (P>0.05) (Fig.10).ConclusionThere were transient cardiac diastolic dysfunction and endothelium-dependent diastolic dysfunction in thoracic aortic within 24 hour after trauma, which might be involved in the secondary cardiac dysfunction induced by non-lethal trauma. |
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