Effects Of HBO Exposure On Cerebral Blood Flow And Apoptosis Of Cerebral Vascular Endothelial Cells In Rabbits

Objective By detecting the effects of hyperbaric oxygen (HBO) exposure on the expressions of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS), Caspase-3 and Bcl-2 mRNA in intemal carotid artery (ICA) and basal artery (BA) of rabbits, we can explore the mechanism of the constriction of the cerebrovascular anterior circulation and dilation of the cerebrovascular posterior circulation, and also the mechanism of the antiapoptotic of the HBO from the level of molecularbiology. Thus to provide the theoretical basis for application of hyperbaric oxygen on brain diseases.Methods Twenty-four healthy adult New Zealand rabbits were randomly divided into 2 groups:the experimental group and the control group, each consisting of 12 animals. The rabbits in the experimental 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 F.Q.PCR method was used to detect variations in the expressions of ET-1, eNOS, Caspase-3 and Bcl-2 mRNA in both ICA and BA in 2 groups.Results HBO can significantly increase the expressions of ET-1 mRNA [(1.679 ± 0.097) vs. (1.000 ± 0.017)] in ICA and eNOS mRNA [(1.667 ± 0.134) vs. (1.000 ± 0.014)] in BA, and decrease the expressions of eNOS mRNA [(0.571 ± 0.039) vs. (1.000 ± 0.023)] in ICA and ET-1 mRNA [(0.565 ± 0.069) vs. (1.000 ± 0.034)] in BA. And also significantly decrease the Caspase-3 mRNA expression [(0.038 ± 0.006) vs. (1.000 ± 0.225)] and increase the Bcl-2 mRNA expression [(1.877 ± 0.169) vs. (1.000 ± 0.364)] in ICA; similarly decrease the Caspase-3 mRNA expression [(0.419 ± 0.091) vs. (1.000 ±0.175)] and increase the Bcl-2 mRNA expression [(1.269 ±0.270) vs. (1.000 ± 0.117)] in BA, all the differences mentioned above were of statistical significance (p< 0.01).Conclusions HBO contracts the cerebrovascular anterior circulation and dilates the the cerebrovascular posterior circulation by regulating the expression of ET-1 and eNOS mRNA in both ICA and BA. And also exerts an inhibition effect on apoptosis in cerebral vascular endothelial cells. The mechanism may be related to inhibiting the expression of Caspase-3 mRNA and promoting the expression of Bcl-2 mRNA.