| Summary: | 碩士 === 國立陽明大學 === 生醫光電研究所 === 102 === The occurrence rate of cardiovascular diseases has remained high in recent decades, if not increasing year by year. The scientific community has put much effort into heart disease research accordingly. In addition, due to the recent rise of tissue engineering research, there has been sufficient evidence showing that mutual action of cells and their surrounding mechanics would cause dysplasia or defect.
In this field, a large number of research groups use drug induced cardiac hypertrophy. Some others apply biochemistry, quantitative measurement on impaired cardiomyocytes and study the hypertrophy signal transmission pathways. However, with this approach, scientists have not been able to figure out if there is any absolute correlation between cardiac hypertrophy and pressure overload. I made a microfluidic cell culture device that could keep cardiomyocytes under hydrostatic pressure similar to human blood pressure, and then used ANP marker to quantify the cardiac hypertrophy levels in the cells. With this approach, I clarify the correlation between pressure overload and cardiac hypertrophy.
I used two drugs ( phenylephrine, isoproterenol ) and pressure overload to induce hypertrophy, both phenylephrine and pressure overload could increase the intracellular level of atrial natriuretic peptide, and the effects of chemical and physical treatments are similar. However, while both phenylephrine and pressure appeared simultaneously, the effect on atrial natriuretic peptide expression was higher than in the case with pressure only, but the cell area is smaller than that induced by the pressure overload. In the case of isoproterenol treatment, however, while both isoproterenol and pressure appeared simultaneously, the effect on atrial natriuretic peptide expression and cell area are smaller than that induced by pressure overload.
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