严重烧伤后心肌钙调节蛋白表达的变化及其信号转导机制

burn shockAlterations of Calcium-regulatory Proteins' Expression and its Signal Transduction Mechanisms in Myocardium after Severe Burns .Burn trauma initiates a pathophysiologic cascade characterized by fluid redistribution, cardiocirculatory insufficiency, and multiple organ failure. Altered vascular tone, cardiac contractile depression and impaired diastolic relaxation have been described after burn trauma in animal models and in humans. Decreased cardiac output was initially attributed to fluid shifts with a resulting hypovolemia and fall in cardiac preload; however, other investigators have attributed postburn cardiac dysfunction to myocardial depressant factors in the serum and lymph, The use of ventricular muscle preparations and isolated cardiomyocytes has confirmed cardiac mechanical dysfunction after a major burn that is intrinsic to the cardiac myocytes. Despite these advances, the cellular mechanisms that contribute to post burn cardiac contractile deficits remain controversial, and recent attention has focused on burn-related changes in intracellular calcium homeostasis. On the other hand, although prompt and adequate fluid resuscitation is desirable after burn injury, this is not always the case. Restoration of blood flow is necessary, but this restoration may lead to a reperfusion injury. Cellular calcium overload and inflammatory myocardial injuries have been attributed to be the main mechanisms of reperfusion injury in myocardial infaraction and cardiac allograft transplantation, which presenting significant advances in our understanding of mechnisms of tissue injury and organ dysfunction resulting from burn shock and delayed fluid resuscitation. However, the cellular signaling mechanisms of calcium overload and signal transduction pathways of inflammatory mediators remain to be elucidated. Our ability to impact outcome through the modification of specific regulators of cellular signaling is promising and deserves the attention of thoughtful critical care surgeons..Sprague Dawley male rats (200～250 g) were randomly assigned to one of each group. Infliction of burn injury was performed on the trunk comprising 30% of the total body surface area by immersion in water at 100℃

研究烧伤休克以及不同复苏条件下心肌细胞膜二氢吡啶受体、肌浆网钙释放通道Ryanodine芴濉⒏票谩⒛聘平换黄鳌⑹芰椎鞍住alreticulin等钙调节蛋白、mRNA表达的变化规律，捌溆肷錾舷偎啬苁芴錭AMP、一氧化氮cGMP系统信号转导变化的相关性，探索严重烧伤后心δ芙档偷姆肿由镅Щ疲罢倚募”；ご胧⑼厣疃孕募∠赴藕抛纪绲娜鲜丁