| Summary: | 碩士 === 東海大學 === 生命科學系 === 103 === Heart failure is defined as a complex clinical syndrome which can result from any structural or functional cardiac disorder that impairs the ability of ventricle to fill with or eject blood. The increased sympathetic activity associated with injury induces distinct changes in the host’s hormonal and immune response and in the coagulation system. A number of synergistic mechanisms are involved in cardiac complications during stress. Epidural anesthesia has been shown to reduce the risk of major postoperative morbidity such as MI (myocardial infarction) or death, however, the underlying mechanism is still unclear. This study was designed to simulate the clinical surgery and spinal anesthesia model in rat to clarify heart injury and the damage recovering mechanism. Oxidative stress related apoptosis and ER (endoplasmic reticulum) stress related autophagy will be monitored in myocardial injury and recovery process. Our preliminary results showed that epinephrine、norepinephrine and NT-proBNP in the blood serum are increased through sympathetic activity in Surgery group, and Marcaine treatment can reverse these changes. We also found that Marcaine treatment can suppress GRP78 and LC3II protein expression which are related to ER stress and autophagy. In conclusion, Marcaine treatment can reduce ER stress induced myocardial apoptosis which was induced after surgery. Additionally, increased mitochondrial area was found in Surgery group, while Marcaine treatment can rescue the mitochondria phenotype. This study demonstrated that giving regional anesthesia may protect patients who are having high risk of heart diseases prior to surgery.
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