| IntroductionThe respiratal-circulatory arrest is the most severe complication during the anesthesia. Even transient arrest may make some injury to the cerebrum, which will result in bad prognosis. Now the study of the machanism of postischemic cerebral injury is based on this three points: (1))the cellular culture; (2)the organ reperfusion; (3)the stream stopping. These methods can obseve the characteristics of the transformation of ischemic cell and the cheef element affect injury, but they cannt evaluate the postresuscitation syndrome and the follow - up re-suite. Not only the ischemia - reperpusion but also the body fluid, intra - environment and other organs could affect the injury of cerebrum. So it is very important to simulate the clinic station of postresuscitate exactely.At present many drugs could do effect on cerebral protection,but it is hard to practice in clinic. The mouse - asphyxia - model is used in this study to simulate the clinical process more exactely and protect more evidence.Ketamine and propofol are widely used in clinic. It has be proved that they could prevent the ischemia - reperfusion injury. The mechanism is: (1)tratso inhibit the production of free - bonds; (2)to clear free - bonds; (3)to inhibit positive gultamine receptor activation. Ketamine is the non - competitive inhibitor of NMDA receptor, thus can inhibit the elevation of the calcium anion in cells. Propofol can do effect on free - bonds and inhibit lipid - over oxidation.The rats - asphyxia - resusciation - model ( MARM) is used in the experiment, use propofol and ketamine to pretreat the rats to study the mechanism of their protective effct on complete ischemia and resuscitation. The indexs are: (1) the SOD activation of cerebrum, pnopylene aldehyde concentration, TNF -a, IL -1b; (2)the IC AM - 1 protein expression and the NF - KB activation in cere-brum; (3)the Bcl - 2 and the Bax gene mRNA expression in cerebrum.Material and methods1. Model building The model is the rats - asphyxia - resusciation - model (MARM) former used in America(1998) , which have been improved.The induction drug is isofluname(4% ) inhalation, the rats are fixef after reflex disappear. After intubation, HAVER - 7000 respiratory machine is used in control - respiration. PETCO2 is 35mmHg-45mmHg( respiratory index; 1ml/ 100g,40time/min) ,maintenance drug is isoflunane (1.5-2.0% ).ECG and tympathenic temperature are detected. The tympathenic tempre-ture is controlled between 37℃-38℃ by lamp.Left femoral vein is intubated and given vecuronium0.02mg/100g and hep-arin 50U/100g. Left femoral artery is intubated 10.0±0.56cm to detect direct centery pressure. Monitoring MAP, HR, ECG and tempreture.Before asphyxia vecuronium(0. 01 mg/100g) and heparin(50U/100g) are injected. Atery blood (0. 25ml/100g) , heparin50U/100g, NaCO3 0. 1mEq/ 100g and adrenalin4ug/100g are mixed in order to be used in resusciation.After these we stop rats from oxygen and shut the tube. Gadiac electronic activity disappeared 2. 51 ±0. 82min later, the MAP is less than 10mmHg. 10min later resusciation drug is given from left femoral artery. At the same time, oxygen supply recovery, 2. 61 ±0. 63min later autonomic circulation recovery. And maintain ventilation till the end, inject 0.9%Nacl 1ml/100g/h during this period.2. Experimental animal allocation Use Wistar rats, male, body weight 160-230g. Fast for 12h before test, and be devided to 4 groups; sham - operation group (group A) ; isoflunane inhalation group (group B) ; propofol group (group C) ; ketamine group (group D). The dose of propofol and ketamine are 10mg/ 100g in peritoneum after induction of group C and D.After experiment, cerebral tissue is taken out immediately and put into 10% formaldehyde and fluid - nitrogen. At the same time artery blood is centrifugatedin 3000r/min for 15min, the above fluid is taken into fluid -nitrogen.3. Dtect index and the methodsDetect index include; (DSOD activations and malonaldehyde concentration in cerebrum at 30, 120, 1...
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