Font Size: a A A

Changes Of Serum Cytokines And Brain Tissue After Cardiac Arrest And The Effect Of Batroxobin

Posted on:2005-08-15Degree:MasterType:Thesis
Country:ChinaCandidate:H CaoFull Text:PDF
GTID:2144360125968360Subject:Emergency Medicine
Abstract/Summary:PDF Full Text Request
Objective To study the changes of blood viscosity,serum cytokines and brain histology in rabbits after cardiopulmonary resuscitation(CPR) and the effect of Batroxobin. To investigate the effect of Batroxobin on neuroprotection and 24h survival rate after CPR. Methods Part one: Modified Pittsburg's model of ventricular fibrillation caused by mechanical discharge was used. Thirty-two rabbits were randomly divided into 3 groups: 8 in sham-operated group(sham),12 in conventional resuscitation group and 12 in Batroxobin group. Sham-operated group was discharged on the chest wall, which did not cause ventricular fibrillation. Rabbits of conventional resuscitation group and Batroxobin group were exposed to 6 min of cardiac arrest(CA) induced by ventricular fibrillation, then conventional resuscitation began. A dosage of 0.3Bu/kg of Batroxobin was given to Batroxobin group at the beginning of resuscitation. The experiment terminated after 12h spontaneous circulation and blood samples were collected for evaluation of TNF-α,NO concentration in serum and blood viscosity. Histology of hippocampus of CA1 region and cerebral cortex were observed by light microscope. Besides, ultramicrostructure of cortex was examined by electronic microscope. Part two: Forty rabbits were randomly divided into 3 groups: 10 in sham-operated group, 15 in conventional resuscitation group and 15 in Batroxobin group. The same model of part one was used without any sample collection. 24h survival rate was observed. Results After CPR ,whole-blood viscosity at high/low shear rate of conventional resuscitation group of both 4h and 12h continuously increased when compared with sham(P<0.05), and the injection of Batroxobin inhibited the increasing(P<0.05), which were significantly different in the three groups(sham,conventional resuscitation group,Batroxobin group)(P<0.05). Plasma viscosity of conventional resuscitation group of both 4h and 12h continuously increased when compared with sham(P<0.05), and Batroxobin inhibited the increasing(P<0.05),especially 12h after CPR when it decreased to sham level. TNF-α concentration in serum increased in both conventional resuscitation group and Batroxobin group 4h after CPR(P<0.05). No significant difference was found between the two groups. 12h after CPR , TNF-α concentration of conventional resuscitation group was higher than 4h after CPR (P<0.05), but it didn't happened in Batroxobin group. Nitric oxide (NO) concentration in serum of both conventional resuscitation group and Batroxobin group increased when compared with sham 4h after CPR(P<0.05),and the concentration of conventional resuscitation group was higher than that of Batroxobin group(P<0.05). Significant different was found in the three groups(P<0.05). 12h after CPR , NO concentration of conventional resuscitation group was higher than 4h after CPR (P<0.05), but it didn't happened in Batroxobin group. Light microscope: Cellular structure of hippocampus of CA1 region and cerebral cortex in sham-operated group was normal on the whole. In conventional resuscitation group, irregular arrangement of pyramidal neurons,cellular edema,nuclear concentration can be observed. Microthrombus can be found in some capillaries . Less severely pathological change was found in Batroxobin group; no microthrombus can be found. Severity of ischemic injury of cortex was in the same turn when observed under electronic microscope. 24h survival rate of Batroxobin group was higher than that of conventional resuscitation group(P<0.10). Conclusion After CPR, whole blood viscosity and plasma viscosity increased; TNF-α,NO concentration in serum increased also. Batroxobin inhibited their increasing after CPR. Batroxobin may released the injury of brain ,raised the 24h survival rate through the above mechanisms.
Keywords/Search Tags:cardiac arrest, blood viscosity, tumor necrosis factor-α, nitric oxide, Batroxobin
PDF Full Text Request
Related items
Effects Of Inducible Nitric Oxide Synthase Expression On Rat Cardiac Fibroblasts Proliferation And Collagen Synthesis And Its Possible Signal Transduction Pathway
The Study Of The Dynamic Changes Of Nitric Oxide And Tumor Necrosis Factor-α Levels Of Plasma In Hypertensive Rats And The Precaution Influence Of These Changes On Cerebrovascular Disease
A Preliminary Investigation Of The Molecular Mechanism Of The Regulation To The Blood-labyrinth Barrier Permeability Of Guinea Pig Inner Ear Affected By Nitric Oxide In Vitro
The Clinical Study Of Endothelin(ET), Nitric Oxide(NO), Tumor Necrosis Factor-α(TNF-α) And Atrial Natriuretic Peptide (ANP) Levels In Blood Of OSAHS Patients With Hypertension
Role Of Tumor Necrosis Factor α And Nitric Oxide In Pathogenesis Of Cerebral Malaria
Effect Of Nitric Oxide On The Injury Of Lung And Heart In Sepsis
Effects Of Nonspecific Nitric Oxide Synthase Inhib Ition On Resuscitation Success And Postresusci Tation Myocardial Dysfunction After Cardiac Arrest In Habbit Models
Effects Of Inhaled Nitric Oxide Combined With Different Concentration Of Oxygen In A Rat Model Of Klebsiella Pneumoniae Pneumonia
The Experimental Study Of Interleukin-10 And Nitric Oxide Inhibiting Activation Of Nuclear Factor-κB And Production Of Tumor Necrosis Factor In Lipopolysaccharide-induced Pulmonary Alveolar Macrophages
10 The Study Of The Relations Between The Dynamic Changes Of Plasma Tumor Necrosis Factor Alpha,Interleukin-6,Interleukin-8 And Nitric Oxide Levels And Hypoxic-ischemic Encephalopathy