Influence of hemodynamics on myocardial cell cardiac index and its molecular mechanism.

With the improvement of people's living standards and change of lifestyles, the morbidity of the cardiovascular and cerebrovascular diseases (cardiovascular and cerebrovascular diseases, CCVD), especially the atherosclerosis (atherosclerosis, AS), presents a rising tendency year by year. The injury and inflammatory reaction of endothelial cells is one of the important factors causing AS. However, its molecular mechanism still needs further studying. This paper will discuss the influence of hemodynamics on the cardiac muscle cells cardiac index and its molecular mechanism. The Human umbilical vein endothelial cells (Human umbilical vein endothelial cells, HUVEC) were cultivated and separated and processed by 100ng Lipopolysaccharide (Lipopolysaccharide, LPS) to simulate the injury and inflammation state of the vascular endothelial cells. The hemodynamic state was simulated by the Parallel-Plate Flow Chamber in laboratory. And the MTT was adopted to detect HUVEC growth and the flow cytometry (flow cytometry, FCT) to detect HUVEC apoptosis. And the cardiac index was tested by RT-PCR and western blot. And the cell apoptosis caused by LPS was tested when the cardiac index was over-expressed and reduced. LPS could inhabit HUVEC growth and lead to its apoptosis. Hemodynamics (16dyn/cm(2)) could reduce HUVEC growth inhibition and apoptosis caused by LPS. And the dose-dependent LPS reduced HUVEC cardiac index, while when it was processed by the hemodynamics (16dyn/cm(2)), the HUVEC cardiac index would increase. And the over-expression of the cardiac index could inhabit the cell apoptosis caused by LPS, and the interference technology was adopted to deal with the cardiac index, which could enhance the cell apoptosis caused by LPS. Hemodynamics could inhabit the HUVEC apoptosis caused by LPS, which might be one of the reasons causing AS, through enhancing the cardiac index.