| 1. BackgroundsThe structure and function of most organs change obviously in the process of aging, and the function reserve of most senile organs becomes- decreased. In this process, the senile lungs become to be vulnerable. In the elderly, pulmonary infection is very prevalent and often complicated with other organ 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 pulmonary infection 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 . Many studies showed that multiple organ failure in the elderly (MOFE) was based on the lung diseases and heart diseases . Renal failure was an important factor of death of MOFE. Many pulmonary infection are induced by gram negative bacteria. Lipopolysaccharide is a main constituent of endotoxin of gram negative bacterium. Through the study of the effects of acute lung injur induced by lipopolysaccharide on cardiac function and renal function of rats with experimental cardiac dysfunction, we may find some clues to understandthe mechanism of multiple organ dysfunction syndrome in the elderly (MODSE) .2. ObjectivesTo observe the effects of acute lung injure on cardiac function and renal function of rats with experimental cardiac dysfunction . To build up some methods to make artificial lung injure animal models ,and to compare these changes with those of normal rats models . To study the mechanism of changes of cardiac function and renal function in the animal models with lung injury and to provide some references to the study of the mechanism of the cardiac functional and renal functional changes in the elderly when infectious lung injury occurs.3. Methods 3.1 Building-up the model of cardiac dysfunctionSixty male Sprague Dawley(SD) rats of 22 month old were randomly divided into 5 groups: the control group, the model groups, the 24 hours group , the 48 hours group and 72 hours group , while sixty male SD rats of 9 month old were divided into 5 groups in the same way . The old and adult rat model with cardiac dysfunction were produced by constricting abdominal aorta : intraperitoneal anesthesia was given with 1.5% mebumal sodium . Abdominal cavity was opend . Aorta and a pointless pip whose diameter is 70% of aorta were ligated with Silk lagation . Then this pointless pip was drawn out so that cross-sectional area of aorta was reduced by 40%-50%. Thirty days later, the rats whose CI value was less then 180ml.min-I.kg-1 were observed .3.2 The acute lung injury inducing the changes of cardiac function and renal function of the rats with the experimental cardiac dysfunction was observedNormal saline was infused into the lungs of the rats of control groups and model groups directly through trachea. The rats of other groups were given lipopolysacchride (LPS) saline suspension by the same methods. On different observed points of time, hemodynamic parameters including heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), the maximal pressure increasing rate during isovolumetric contration phase ( + dp/dtmax), the maximal pressure decreasing rate during isovolumetric relaxation phase ( -dp/dtmax), and Vmax value were measured by the method of catherization; blood gas analysis and the blood levels of tumor necrosis factor-a (TNFa), soluble intercellular adhesion molecule (sICAM-1) , Interleukin-1 (IL-1), Interleukin-6 (IL-6), nitric oxide (NO), endothelin (ET) were determined; heart, kidney and lung morphological structure were observed by microscope and electron microscope. The TNF-a protein , inducible nitric oxide synthase (iNOS) protein , ICAM-1 protein in pulmonary , renal and myocardial tissue were observed with immunohistochemical analysis respectively; and iNOS protein, ICAM-1 protein in rena...
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