Changes Of Cytokine,p38MAPK And The Effects Of Drugs During Cardiopulmonary Cerebral Resuscitation Rats

Moer attention is payed how to enhence the survival rate and quality of life after CPCR of CA patient. In the past few years the role of inflammatory is valued in CPCR, the negative contribution of tumor necrosis factor–αand interleulin-1βhave been accredited generally after ischemic of cardia and brain. At the same time, orther cytokine(ICAM-1,MMP-9,TGF-β1) and p38MAPK were expressed and activated in CPCR, they promote each other and enhance damage of brain and cardia. Along with the development of the theories and the methods of CPCR, epinephrine has been administed as a drug essential for CPCR. Especially, high dose epinephine may enhance the success rate of resuscitation of sudden CA. However, many investigations were demonstrated that high dose epinephrine may result in more serious sequela and reduce the survival rate after CA. If the excessive inflammatory reaction are inhibited after CPCR, the success rate of resuscitation of sudden CA will been elevated. The motive of experiment①Content of cytokine (IL-1β,TNF-α,ICAM-1, MMP-9,TGF-β1),activated p38MAPK are observed in tissue of cardia and brain, thuough erect model of CPCR rats.②Contribution of cytokine (IL-1β,TNF-α,ICAM-1,MMP-9,TGF-β1),activated p38MAPK and the ultrstructure in brain and cardia are observed after treatment with different dose of Xue bi jing.Methods Fifty Wistar rats(body weight 300±20g) were divided into five groups at random,ten rats each groups. Besides control guoup, the rest treat with routine method after AC.1.Control group: only to be intubatede, not choked. 2.Model group:to cause to happen model of AC, and treat with Sodium Chloride (5ml.Bid) aftet successful resuscitation.3, Little dose of xue bi jing group: to cause to happen model of AC, and treat with Xue bi jing (5ml/kg) diluted 5ml.i.vBid three day before resuscitation and one day aftet successful resuscitation . 4.Middle dose of xue bi jing group: to cause to happen model of AC, and treat with Xue bi jing (7.5ml/kg) diluted 5ml.i.vBid three day before resuscitation and one day aftet successful resuscitation . 5. High dose of xue bi jing group: to cause to happen model of AC, and treat with Xue bi jing (15ml/kg) diluted 5ml.i.vBid three day before resuscitation and one day aftet successful resuscitation .Results 1. Contents of cytokine ( IL-1β,TNF-α,ICAM-1,MMP-9,TGF-β1),activated p38MAPK in cardia and brain of rats increase obviously after 24 hours resuscitation. 2.Xue bi jing significantly inhibit the quantitation of cytokine (IL-1β,TNF-α,ICAM-1,MMP-9),activated p38MAPK expression from CPCR rats, dose decide effect. 3. Compare with contral group the ultrstructure of brain and cardia were damadged in orther groups, compare with contral group the level of cytokine ( IL-1β,TNF-α,ICAM-1,MMP-9,TGF-β1) and activated p38MAPK were increase significantly in the brain and cardia of model group.Conclusion 1. Contents of cytokine (IL-1β,TNF-α,ICAM-1,MMP-9,TGF-β1) and activated p38MAPK in cardia and brain of rats increase obviously after 24 hours resuscitation, and over increased cytokine(IL-1β,TNF-α,ICAM-1,MMP-9) and activated p38MAPK injure brain and cardia of rats.2. Xue bi jing significantly inhibit the quantitation of cytokine (IL-1β,TNF-α,ICAM-1,MMP-9) expression and activated p38MAPK from CPCR rats, increased TGF-β1, and lessen tissue damage.3. Xue bi jing significantly inhibit the quantitation of cytokine (IL-1β,TNF-α,ICAM-1,MMP-9) expression and activated p38MAPK from CPCR rats, dose decide effect, high dose xue bi jing reduce the damadge led by ischemia/reperfusion from CPCR rats more obvious than other dose.