| 1. BackgroundsThe structure and function of most organs change obviously in the process of aging, and the function reserve of most senile organs become decreased. In this process, the senile lungs become to be vulnerable. In the elderly, pneumonia is very prevalent and often complicated with other organs dysfunction or even failure. It is also one of the common causes of death in the elderly. But the mechanism of multiple organ dysfunction (or failure) induced by pneumonia in the elderly is still not very clear. In previous reports, heart events get frequent and the death rate caused by heart events is much higher when pneumonia occurs in the elderly, however the mechanism remains unclear.2. ObjectivesTo build up some methods to make artificial accelerated aging animal models and artificial lung infection animal models, to observe the changes in cardiac function related parameters induced by pneumonia in aging rodent models, and to compare these changes with those of normal rodent pneumonia models. To study the mechanism of cardiac function changes in the artificial aging animal models with pneumonia and to provide some references to the study of the mechanism of the cardiac function changes in the elderly when pneumonia occurs.3. Methods3.1 The difference of cardiac function changes induced by pneumonia between normaland D-galactose pretreated ratsFifty-two normal male SD rats were divided into two groups randomly. One group was treated with D-galactose by subcutaneous injection (D-gal group), and the other group was treated with normal saline by subcutaneous injection (NS group). Then, 16 rats of each groups were injected pseudomonas aeruginosa saline suspension directly through trachea to induce pneumonia. The other rats were injected with normal saline to be used as control. Then, murine hemodynamics including heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), the maximal pressure increasing rate during isovolumetric contraction phase (+dp/dtmax), the maximal pressure decreasing rate during isovolumetric relaxation phase (-dp/dtmax), and T value were observed respectively in 24 hours and 72 hours after pneumonia was induced. At the end of the experiment, blood gas analysis and tumor necrosis factor- a (TNF- a) measurement were performed. Some cardiac tissues were also observed by microscope and electron microscope.3.2 The changes of some materials in the heart of artificially accelerated aging mouse models with pneumoniaSome normal male NIH mice were divided into two groups randomly. One group was pretreated with D-galactose by subcutaneous injection (D-gal group), and the other group was pretreated with normal saline by subcutaneous injection (NS group). Then, some mice of each group were injected pseudomonas aeruginosa saline suspension directly through trachea to induce pneumonia. The other rats were injected with normal saline to be used as control. Then mice were killed in 24 hours and 72 hours after pneumonia was induced, and some measurements were performed, and the measured parameters included plasma level of TNF- a , the heart tissue content of Adenosine Triphosphate (ATP), TNF- a and malondialdehyde (MDA), the activity of total Superoxide Dismutase (T-SOD), Gu,Zn-SOD, Nitric Oxide Synthase (NOS), theexpression changes of Gu^n-SOD mRNA and TNF- a rnRNA in the heart tissue. Some cardiac tissues were also observed by immunohistochemical analysis, microscope and electron microscope.3.3 The influence of melatonin on the changes of some materials in the heart of artificially accelerated aging mouse models with pneumoniaIn this part, D-galactose pretreated and normal mice were randomly divided into 2 groups respectively. They were injected with normal saline (the normal group) or pseudomonas aeruginosa saline suspension directly through trachea (the others group) to induce pneumonia. Then each group was divided into four subgroups, i.e. the control group, 3-day pneumonia group, MT-pneumonia grou... |
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