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Objective To investigate the effect of propofol on the expression of c-fos protein and c-fos mRNA in hippocampus during global cerebral ischemia-reperfusion in rats. Methods Forty male Wistar rats weighing 250-320 g were randomly allocated to one of five groups: group A received sham operation ( n = 8); group B received ischemia-reperfusion (I-R n = 8); group C received intraperitoneal propofol 50 mg?kg-1(C1 n = 8) or 100 mg@kg-1(C2 n = 8) or 150 mg2kg-1(C3 n = 8) 10 min before I-R. The animals were anesthetized with intraperitoneal pentobarbital 40 mg?kg-1.Vertebral arteries were surgically exposed and permanently occluded by coagulation. Bilateral common carotid arteries were exposed. 4-0 silk suture was placed around the arteries. Global cerebral ischemia was induced by lighting the suture for 10 min which was then loosened for reperfusion. At the end of 60 min reperfusion the animals were decapitated on ice and brain was immediately removed. Different brain tissues were either kept in liquid nitrogen ( - 80℃) or fixed in 10% formalin. The changes in c-fos protein in brain was evaluated by immuno-histochemical methods and c-fos mRNA expression in hippocampus was detected using semiquantitative RT-PCR technique.Results The c-fos expression was minimal in sham operation group. I-R induced significant increase in the expression of c-fos protein and c-fos mRNA and propofol significantly inhibited the increase in c-fos expression induced by I-R. The levels of c-fos expression were higher in group C1 than that in group C2 (P 0.05) . Conclusion The study shows that propofol can significantly inhibit expression of c-fos protein and c-fos mRNA induced by global cerebral I-R.
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Objective To investigate the effects of esmolol on ATPase activity in myocardial mitochondria after resuscitation in rats.Methods Sixty-six male Wistar rats were randomly allocated to three groups:sham group,AD group,AD+Es group.A cardiac arrest model was reproduced by asphyxiation in rats,and then CPR was performed in these animals after 10min asphyxia.The ATPase activity of myocardial mitochondria was determined at 30th,120th and 180th minute after resuscitation.ECG,MAP,HR and temperature were measured continuously.Results Heart rates were significantly higher after adrenaline when compared with sham group.Myocardial mitochondria ATPase activity was decreased significantly in both AD and AD+Es group compared with that of sham group(P
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Objective To investigate the cerebral protective effects of propofol and ketamine against ischemia-reperfusion injury induced by cardiac arrest in rats. Methods One hundred and twenty male SD rats weighing 180-250 g were randomly divided into four equal groups of 30 animals : group A served as control without cardiac arrest;group B was subjected to 10 minutes of cardiac arrest followed by resuscitation ( C-R); group C received propofol 10 mg 100 ?g-1 ip 10 min before C-R; group D received ketamine 10 mg-100? g-1 ip 10 min before C-R. The animals were anesthetized with isoflurane inhalation by mask, intubated and mechanically ventilated. Anesthesia was maintained with isoflurane inhalation. Cardiac arrest was induced by asphyxiation (vecuronium 0.01 mg - 100 g -1, disconnection of ventilator, tracheal tube clamping) and maintained for 10 min, then resuscitated. Seven animals in each group were killed at 30 min (T, ) , 120 min (T,) and 180 min (T3 ) after successful resuscitation respectively for determination of serum TNF-a and IL-Ip and cerebra) SOD activity and MDA content. Results Cerebral SOD activity in group C and D was significantly lower than that in group A but higher than that in group B, while cerebral MDA content in group C and D was significantly higher than that in group A but lower than that in group B ( P