2003Zhonghua mazuixue zazhiRequires access

Cerebral protective effects of propofol and ketamine against ischemia-reperfusion injury in rats

Jia You

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Abstract

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 0.05 or 0.01) . Serum TNF-a and IL-Iμ levels were significantly increased in group C and D at T, and T, ( P 0.01). Conclusion Propofol and ketamine can protect brain against ischemia-reperfusion injury through their anti-oxidant and anti-inflammatory effects.

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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 0.05 or 0.01) . Serum TNF-a and IL-Iμ levels were significantly increased in group C and D at T, and T, ( P 0.01). Conclusion Propofol and ketamine can protect brain against ischemia-reperfusion injury through their anti-oxidant and anti-inflammatory effects.

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Available abstract

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 0.05 or 0.01) . Serum TNF-a and IL-Iμ levels were significantly increased in group C and D at T, and T, ( P 0.01). Conclusion Propofol and ketamine can protect brain against ischemia-reperfusion injury through their anti-oxidant and anti-inflammatory effects.

Key concepts: Isoflurane, Propofol, Ketamine, Anesthesia, Medicine, Ischemia, Inhalation, Resuscitation

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