| PrefaceOn the basis of primary progress of clinical and experimental research in the multiple organ failure in the elderly (MOFE), the multiple organ dysfunction syndrome in the elderly (MODSE) recently has attracted more attention. With the decay of organ function by the ageing and by the chronic diseases, the organs in old persons are almost at the threshold of dysfunction. Because of some less intense irritation, two and more organs present sequential and/or simultaneous dysfunction in a short time, which is the key reason that induced death in critically ill old patients.The theory 'gut motor' has taken the predominant position in recent three decades. The translocation of bacteria from the intestinal tract, the 'intestine in shock' represents the trigger reaction that eventually leads from the 'organ in shock', early organ failure to late (septic) organ failure. Some researchers think that the gut is the "motor" of such septic states and the first step of a "gut-liver-lung axis". Shock of any type or sepsis can by themselves lead to increased permeability of the intestinal mucosal barrier. This, in turn, may promote bacterial translocation, i.e. the passage of bacteria or bacterial products such as endotoxin from the lumen of the gut into the portal bloodstream. When such products reach the liver, activation of Kupffer cells occurs, resulting in the secretion of proinflammatory and hypotensive mediators. Although the gut motor impressed a lot of investigators, this theory can't explain perfectly the process of MODS induced by shock and sepsis. In clinical experience, it was found that in MODS in the elderly (MODSE), the lung is often the first organ to fail and pneumonia is the common predisposing factor for ARDS, which can serve as the initial manifestation of the MOF. In clinic, pneumonia that necessitates ICU admission leads to ARDS in approximately 10% of patients. In endotoxin and low perfusion induced MOF in aged rat, often the lung is involved initially. Recently, investigators use intraperitoneal injection of the inflammatory agentZymosan to elicit a systemic inflammatory response that mimics MOF. So lung may be a motor organ of MODSE in some cases.Despite the potent effects of endotoxin on neutrophils, the initial effector cell of endotoxin-induced organ injury is probably the tissue macrophage. This cell and monocyte produce many inflammatory mediators and respond to endotoxin by quickly producing large amounts of tumor necrosis factor a (TNF- a ) and interleukin (EL) 1, which have been considered a central mediator of septic shock. TNF- a and IL-1 produce beneficial and deleterious roles in the body. On the one hand, TNF- a and IL-1 play beneficial roles by producing acute phase proteins against protease function by IL-6; IL-4, IL-10, soluble Tumor necrosis factor receptor I and n (sTNFR I-II) and IL-1 receptor a (IL-IRa) against proinflammatory cytokines. Macrophages, Lymphocytes(T and B) and Neutrophils can directly clear endotoxin. On the other hand, TNF- a and EL-1 play deleterious roles by producing IL-8, platelet-activating factor(PAF), complement, histamine, thrombomodulin; directly injure microcirculation and pivotal organs. An appropriate systemic inflammatory response occurs both in MOF and MOFE, which is termed as systemic inflammatory response syndrome (SIRS). The balance between the beneficial and deleterious role determine the prognosis of the body. If the beneficial roles take the predominant position, the patient will reach recovery, and vice versa, MOF and MOFE will occur.The underlying mechanism of heart failure is still not sure in SIRS. Our study is conducted to explore the injury and potential mechanism on aged cardiomyocytes of TNF- a by the changes of mitochondria membrane potential, cytolic calcium concentration [Ca2+]i, transcription factor nuclear factor (NF)- K B, heat shock protein 70 and bcl-2.Part IThe establishment of senescence cardiomyocytesObjective: To establish senescence cardiomyocytes in vitro.Methods: The cardiomyocytes were harv...
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