ABSTRACT
Compared with conventional cardiopulmonary resuscitation (CCPR), extracorporeal cardiopulmonary resuscitation (ECPR) can improve the survival rate of patients with cardiac arrest, and reduce the risk of reperfusion injury. However, it is still difficult to avoid the risk of secondary brain damage. Low temperature management has good neuroprotective potential for ECPR patients, which minimizes brain damage. However, unlike CCPR, ECPR has no clear prognostic indicator. The relationship between ECPR combined with hypothermia management-related treatment measure and neurological prognosis is not clear. This article reviews the effect of ECPR combined with different therapeutic hypothermia on brain protection and provides a reference for the prevention and treatment of neurological injury in patients with ECPR.
Subject(s)
Humans , Brain , Cardiopulmonary Resuscitation , Brain Injuries , Hypothermia, Induced , Heart ArrestABSTRACT
Objective To investigate the establishment of focal cerebral ischemia model in rabbits with the improved suture method.Methods A total of 45 healthy and clean adult New Zealand rabbits were divided into either a sham operation group (n =5) or a model group (n =40) using random number table method before modeling,and the sex was not limited.The self-made head ends of 2-0 fishing lines dipped in paraffin were used as the sutures.The external carotid artery was cut and inserted into a intracranial artery through the internal carotid artery and blocked the origin of middle cerebral artery.The neurological function score was performed after 6 h.The neurological deficit scores ≥2 was successful modeling.The rabbits were killed by anesthesia.The brain slices were stained with 2％ 2,3,5-triphenyl tetrazolium chloride solution.The infarct foci were observed.The diameters of suture head and the depth of suture insertion were compared in the model rabbits with successful modeling,failure,and death in the model group.Results There were 40 rabbits in the model group,six of them died,including 4 died of subarachnoid hemorrhage within 4 h after operation,and 2 died from anesthetic accident.The mortality rate was 15.0％.Seven rabbits failed,mainly because of cerebral vasospasm and the insertion depth of suture was insufficient.Twenty-seven had successful modeling,and the success rate was 67.5％.All the rabbits in the sham operation group survived.The diameter of the suture head and insertion depth in the successful modeling rabbits were compared with the death and failure outcome in rabbits.The difference was statistically significant (diameter:0.52 ± 0.14 mm vs.0.45 ±0.40 mm and 0.58 ±0.17 mm;depth:5.49 ±0.17 cm vs.6.04 ± 0.11 cm and 4.26 ±0.30 cm;all P ＜ 0.05).Conclusions The improved suture method can successfully prepare the focal cerebral ischemia model of middle cerebral artery in rabbits.The method is simple.Its repeatability and practicability are better.
ABSTRACT
Objective To investigate the effects of hyperbaric Oxygen (HBO)exposure on Caspase-3 and Bcl-2 mRNA ex-pressions in both internal carotid artery (ICA)and basal artery (BA)in rabbits.Methods Twenty-four healthy adult New Zealand rabbits were randomly divided into 2 groups:HBO group and the control group,with each group consisted of 12 animals.The rab-bits in the HBO group were exposed to HBO at 2.2 ATA for 60 minutes each day for 3 successive days.The rabbits in the control group were normally fed without any treatment.Real-time PCR was used to detect Caspase-3 and Bcl-2 mRNA expressions in both ICA and BA in 2 groups.Results HBO significantly decreased the Caspase-3 mRNA expression [(0.038 ±0.006 )vs .(1.000 ± 0.225)]and increased the Bcl-2 mRNA expression [(1.877 ±0.1 69)vs .(1.000 ±0.364)].In ICA,HBO similarly decreased the Caspase-3 mRNA expression [(0.41 9±0.091)vs .(1.000 ±0.1 75)]and increased the Bcl-2 mRNA expression [(1.269 ±0.270) vs .(1.000±0.1 1 7)]in BA.All the differences mentioned above were of statistical significance (P <0.01).Conclusion HBO ex-erts an inhibition effect on apoptosis in cerebral vascular endothelial cells.The mechanism may be related to inhibiting the expres-sion of Caspase-3 mRNA and promoting the expression of Bcl-2 mRNA.