| Background: With the development of modern society, the incidence of traumatic shock resulting from traffic accidents and natural disasters has increased and become one of the main causes of death. Multiple factors participate in process of development of shock. Experts from home and aboard have made deeply research on the pathogenesis of shock on the level of molecule and found that many cytokines and inflammatory media participate in the processes of traumatic shock. But the therapy on shock, especially on severe shock is difficult for traumatic shock is a complicated pathophysiologial process influenced by multiple factors, and the real mechanisms is unclear at present. In view of this status, we have made research on the changes of adrenomedullin in rats with traumatic shock.AM is a sort of decompression polypeptide , first found in 1993, which participates in the regulatory process of many pathophysiological activities as a sort of novel hormone. Any of TNF, lipopolysaccharide and IL-1B can stimulate VSMC to produce AM. The primary role of AM is to distend blood vessel and decrease blood pressure, and it can also restrain the migration of vessel smooth muscle cells. AM can take part in the regulation of blood vessel activity and stress, and it plays an important role in pathological conditions such as shock, hypertention, heart failure and renal failure.More researches have been made on adrenomedullin in septic shock and hemorrhagic shock than in traumatic shock. Multiple cytokines and inflammatory media which have been released by traumatic organs play an critical role in the processes of pathophysiological activities during traumatic shock. It have very important significance in clinic so we study the alteration,mechanism and the correlative therapy of AM to curing the traumatic shock,especially for severe shock.Objectives1 The animal model of traumatic shock in rat was made to investigate thedynamic changes and mechanism of AM . To reveal the internal contactduring the process of development of shock and offer new ideas for thepathogenesis with traumatic shock.2 In order to provide a new way for clinical therapy and to investigate theaction and mechanisms of adrenomedullin during traumatic shock, thedistribution, alteration of AM in important organs were observed.3 To observe the correlation between AM and NO. It has been shown thatAM is activated by NO during the traumatic shock. To reveal the changes ofcytokines during the process of shock and offer new ideas for thepathogenesis with traumatic shock, which would provides experimentalfoundation for selecting the new way for clinical therapy.Methods and Results1. The dynamic change of the concentration in plasma of AM duringtraumatic shock.A rat traumatic shock model was made by fracturing bilateral thighbone. SD rats 30 were randomly allocated into control group (CG 10), traumatic shock without resuscitation group (TSWRG 10), traumatic shock on resuscitation group (TSORG 10) and aminoguanidin group AG(G 10). The change of MAP and concentration in plasma of AM were recorded in each group. Within 2 hours is considered early period and after shock 2 hours is considered late period. Concentration of plasma of AM is detected by method of radio-immunoassay. The results showed that concentration ofplasma of AM increased evidently in early and late period during traumatic shock, especially in earlier period. In our experiments, concentration of plasma of AM in TSWRG and TSORG were significantly increased compared with control group at each point after shock, then decreased by degrees followed the shock. Concentration of plasma of AM of TSORG decreased faster than TSWRG within 0.5~2h after shock. 2 The dynamic changes of the concentration in organs of AM during traumatic shock.A rat traumatic shock model was made. SD rats 40 were randomly allocated into 4 groups: control group 10 rats, after shock 30min 10 rats, after shock 3h 10 rats, after shock 5h 10 rats . Distribution and alteration of AM in liver, lung a...
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