Effects of mild hypothermic cardiopulmonary bypass on neuronal apoptosis in hippocampus CA1 region in rats
- VernacularTitle:中低温体外循环对大鼠海马CA1区神经元凋亡的影响
- Author:
Tingjie ZHANG
;
Yannan HANG
- Publication Type:Journal Article
- Keywords:
Hypothermia, induced;
Cardiopulmonary bypass;
Hippocampus;
Neurons;
Apoptosis
- From:
Chinese Journal of Anesthesiology
1996;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of mild hypothermic cardiopulmonary bypass(CPB) on bax and bcl-2 protein expression and neuronal apoptosis in hippooampus CA1 region in rats. Methods Healthy male SD rats weighing 380-420g were randomly divided into 3 groups: (1)post-CPB 1h group (n=6); (2) post-CPB 6h group (n=6) and (3) sham CPB group(n=5). The animals were anesthetized with intraperitoneal fentanyl 150?g?kg~(-1), midazolam 1 mg?kg~(-1) and vecurunium 0.1 mg?kg~(-1), intubated and mechanically ventilated. Left femoral artery was cannulated for heparinizafion, BP monitoring and blood sampling. Artery in the tail and right jugular vein were cannulated for CPB. The animals in group 1 and 2 underwent 2 h mild hypothermic (26-28℃) CPB at a flow of 160 ml?kg~(-1)?min~(-1). 1h(group 1) and 6h(group 2) after CPB 4% polymerized formaldehyde was injected via the artery in the tail. Brains were immediately removed. Bax and bcl-2 protein expression in hippocampus CA1 region was determined by immuno-histochemistry method and neuronal apoptosis by TUNEL technique. Ultrastructural changes were examined with electron microscope. Results (1)Bax and Bcl-2 protein expressions were significantly higher in group 1(1h after CPB)than in sham CPB group. Bax protein expression was significantly higher but bcl-2 protein expression was significantly lower in group 2 than in group 1. bax/bcl-2 ratio in group 2(at 6h after CPB)was significantly higher than that in group 1(at 1h after CPB). (2) Neuronal apoptosis was significantly increased in group 1 and 2 compared to sham CPB group. (3) Electron microscopy showed that some mitochondria were moderately or severely swollen with vacuolizafion and decreased number of mitochondrial at 1h after CPB and at 6h after CPB there was shrinkage of neuronal cells with irregular shape of nucleus, notches in nuclear membrane and margination of nucleoli. Conclusion CPB induces upregulation of both bax and bcl-2 protein expression with predominance of the pro-apoptotic gene Bax leading to increased neuronal apoptosis, indicating that CPB can cause brain injury.
