| Factors like serious inflammation, injury, burn, shock, surgical operation, etc. may cause endotoxin to get into the blood directly or indirectly through the dislocation of enterogenous endotoxin, thus resulting in endotoxemia (ETM). This is a very common and complicated problem faced by modern medical science concerning clinic serious and dangerous diseases and also a difficult point directly affecting the after-recovery and treatment result of the patient. If ETM cannot be discovered as early as possible and given effective treatment, the inflammatory reaction of patient's organs will be aggravated and worsened continuously and even further developed into endotoxin shock and multiple organ dysfunction syndromes (MODS) that might be fatal to him or her. As a result, it is undoubtedly of great theoretical and clinic significance to strengthen the study of ETM.Over recent years, the study of ETM is mostly focused on the generation of inflammatory medium TNF- a and its damage to liver, lung and kidney tissues of the body but the study on myocarditic damage is less reported. Nevertheless, the heart is also a potential place where the inflammatory medium is generated. Factors such as heart transplantation, circulation in vitro may induce the rise of the endotoxin within the body initiating myocarditic inflammatory reaction, further leading to the clinic syndromes similar to heartfailure, and even worsened into cardiogenic cachexia. Moreover, consecutive hypotension caused by endotoxin may lead to myocarditic ischemia and direct pathological damage of LPS to myocardium. Hence, it is mandatory to deepen the study of the impact of ETM on myocardium.At present, it is considered that endotoxin solely plays a trigging role in the attacking process of ETM. The excessive inflammatory media generated by its stimulation is the key problem with the induction of the complete inflammatory reaction of the whole body and the organ function damage. In numerous inflammatory cell factors, TNF- a may play a core role. It not only introduces multiple biological activities of endotoxin but also extends biological effects through the induction of coordinating activities of other media and participates in the inflammatory reaction and tissue damage from different links. Studies have demonstrated that IL-1 plays an important role in the generation and development of ETM as well. When an organ is affected by factors like bacteria, endotoxin, TNF, etc, EL-1 in local structure and blood circulation is increased abnormally and with the coordinating effect of factors such as TNF-a, IL-6, etc. brings about fever, acute reaction and cachexia of the organ. The latest studies have shown that the high mobility group-1 protein (HMG-1) could be one of potential late-stage media in the pathological process of ETM and also an important reason for endotoxin to cause the death of animals. But this still needs to be proven further.The pathogenic mechanisms of ETM are very complicated. There have been no satisfactory results of its treatment. At the present, the comprehensive therapy is being adopted, inhibiting excessively released inflammatory media in a multi-link and multi-level way, actively supplementing endogenous inhibitorsor immunomodulators, and simultaneously searching for more reasonable and treatment measures and more powerful interference ways. Over past few years, studies have denoted that pentoxifylline (PTX) has a selective anti-inflammatory effect and is able to produce a beneficial protective effect on the ETM-affected organ. In the in vivo and in vitro experiments of rats, PTM is able to significantly inhibit the generation of TNF- a induced by endotoxin. Its application perspective is optimistic. It is possible for PTX to become a new effective medicine for curing ETM.The present experiment mainly investigates the generation and change of important inflammatory media (TNF-a , IL-1 and HMG-1) of rats, and the inhibition of inflammatory media and protective effect of PTX. 60 healthy male SD rats were random...
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