Hyperoxia Management During Deep Hypothermia for Cerebral Protection in a Circulatory Arrest Rabbit Model_Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Authors：

WANG Qian , YANG Jiuguang , LONG Cun

Department of Extracorporeal Circulation, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences &;
Peking Union Medical College, Beijing 100037, P. R. China;;

Corresponding author：

Keywords：

Hyperoxia management; Deep hypothermic circulatory arrest; Antegrade selective cerebral perfusion; Cerebral protection; Rabbit

Video：

Export PDF Favorites Scan Get Citation

Abstract Full text Figures/Tables Video References Cited by

Abstract： Objective To investigate the cerebral protective effects of hyperoxia management during deep hypothermia circulatory arrest（DHCA） rabbit by the blood gas indexes, superoxide dismutase（ SOD） activity and malondialdehyde （MDA） levels of brain, and ratio of water to brain. Methods A DHCA and antegrade selective cerebral perfusion （ASCP） rabbit model was established. Twenty-four 11-13 week-old male New Zealand rabbits（ weighing 2.7 to 3.4 kg） were assigned to three groups with a random number table: a sham operation group （Sham group）, an ASCP group （S group）, and an ASCP ＋ hyperoxia management group （SH group）. There were eight rabbits in each group. We recorded the intraoperative values for arterial oxygen pressure （PaO2）, arterial oxygen saturation （SaO2）, jugular venous oxygen pressure（PjvO2）, jugular venous oxygen saturation（ SjvO2） and blood lactate level. The brain SOD activity, MDA levels, and ratio of water to brain were measured after the operation. Results Before initiating circulatory arrest, before initiating reperfusion and five minutes of reperfusion, levels of PaO2 , PjvO2 , and SjvO2 in the SH group were significantly higher than those of the S group and Sham group. SOD activity in the SH group was not significantly different from that of the S group[（213.53±33.52） U/mg. prot vs. （193.02±27.67） U/mg. prot] and Sham group[（213.53±33.52） U/mg. prot vs.（244.38±35.02）U/mg. prot], but the SOD activity in the S group was lower than that in the Sham group（ P ＜ 0.05）. MDA levels in the SH group were lower than that in the S group[（1.42±0.30） nmol/mg. prot vs. （2.37±0.55） nmol/mg. prot, P ＜ 0.05]. Conclusion Our data show that hyperoxia management during DHCA＋ASCP improves rabbits’PjvO2 and SjvO2, maintains brain SOD activity, and decreases brain MDA levels, demonstrating the neuroprotective effects of hyperoxia mangagement.

Citation： WANG Qian,YANG Jiuguang,LONG Cun,et al.. Hyperoxia Management During Deep Hypothermia for Cerebral Protection in a Circulatory Arrest Rabbit Model. Chinese Journal of Clinical Thoracic and Cardiovascular Surgery, 2012, 19(1): 57-61. doi: Copy

1.	Griepp RB. Cerebral protection during aortic arch surgery．J Thorac Cardiovasc Surg, 2001, 121(3)：425-427.
2.	Harrington DK, Fragomeni F, Bonser RS. Cerebral perfusion. Ann Thorac Surg, 2007,83(2)：S799-S804.
3.	杨九光, 龙村, 姚忠喜, 等．经右锁骨下动脉、右房插管兔体外循环及选择性脑灌注模型的建立．中华实验外科杂志, 2000,17(1)：77-78.
4.	杨九光, 龙村, 孙立忠, 等．全主动脉弓置换术中的温度管理．中国胸心血管外科临床杂志, 2005,12(5)：312-315.
5.	田良鑫, 孙立忠, 程卫平, 等. 单侧与双侧顺行性脑灌注对认知能力的影响. 中国胸心血管外科临床杂志, 2005,12(1)：8-10.
6.	Joachimsson PO, Sjöberg F, Forsman M, et al．Adverse effects of hyperoxemia during cardiopulmonary bypass．J Thorac Cardiovasc Surg, 1996, 112(3)：812-819.
7.	Dexter F, Kern FH, Hindman BJ, et al．The brain uses mostly dissolved oxygen during profoundly hypothermic cardiopulmonary bypass. Ann Thorac Surg, 1997, 63(6)：1725-1729.
8.	Nollert G, Nagashima M, Bucerius J,et al．Oxygenation strategy and neurologic damage after deep hypothermic circulatory arrest. Ⅰ.Gaseous microemboli. J Thorac Cardiovasc Surg, 1999,117(6)：1166-1171.
9.	Leyvi G, Bello R, Wasnick JD, et al．Assessment of cerebral oxygen balance during deep hypothermic circulatory arrest by continuous jugular bulb venous saturation and near-infrared spectroscopy. J Cardiothorac Vasc Anesth, 2006, 20(6)：826-833.
10.	Cormio M, Valadka AB, Robertson CS．Elevated jugular venous oxygen saturation after severe head injury．J Neurosurg , 1999, 90(1)：9-15．.
11.	Croughwell ND, Newman MF, Blumenthal JA, et al．Jugular bulb saturation and cognitive dysfunction after cardiopulmonary bypass. Ann Thorac Surg,1994, 58(6)：1702-1708.
12.	Young C，Tenkova T, Dikranian k，et a1．Excitotoxic versus apoptotic mechanisms of neuronal cell death in perinatal hypoxia／ischemia．Curr Mol Med，2004, 4(2)：77-85．.
13.	Liu Y, Rosenthal RE, Haywood Y, et al．Normoxic ventilation after cardiac arrest reduces oxidation of brain lipids and improves neurological outcome. Stroke, 1998, 29(8)：1679-1686.
14.	Kilgannon JH, Jones AE, Shapiro NI, et al．Association between arterial hyperoxia following resuscitation from cardiac arrest and inhospital mortality. JAMA, 2010, 303(21)：2165-2171.
15.	McCord JM, Fridovich I．Superoxide dismutase. J Biol Chem, 1969, 244(22)：6049-6055.
16.	Lewén A, Matz P, Chan PH．Free radical pathways in CNS injury. J Neurotrauma, 2000, l7(10)：871-890.
17.	Kamada H, Yu F, Nito C, et al．Influence of hyperglycemia on oxidative stress and matrix metalloproteinase-9 activation after focal cerebral ischemia/reperfusion in rats：relation to blood-brain barrier dysfunction. Stroke, 2007,38(3)：1044-1049.
18.	Maier CM, Hsieh L, Crandall T, et al．Evaluating therapeutic targets for reperfusion-related brain hemorrhage. Ann Neurol, 2006, 59(6)： 929-938.
19.	Narasimhan P, Liu J, Song YS, et al．VEGF stimulates the ERK 1/2 signaling pathway and apoptosis in cerebral endothelial cells after ischemic conditions. Stroke, 2009, 40(4)： 1467-1473.
20.	祝忠群, 朱德明, 苏肇伉, 等．先天性心脏病儿体外循环的再氧合损伤．中国体外循环杂志, 2005,3(3)：131-133.
21.	Pearl JM, Thomas DW, Grist G, et al．Hyperoxia for management of acid-base status during deep hypothermia with circulatory arrest. Ann Thorac Surg, 2000，70(3)：751-755.

1. 　Griepp RB. Cerebral protection during aortic arch surgery．J Thorac Cardiovasc Surg, 2001, 121(3)：425-427.
2. 　Harrington DK, Fragomeni F, Bonser RS. Cerebral perfusion. Ann Thorac Surg, 2007,83(2)：S799-S804.
3. 　杨九光, 龙村, 姚忠喜, 等．经右锁骨下动脉、右房插管兔体外循环及选择性脑灌注模型的建立．中华实验外科杂志, 2000,17(1)：77-78.
4. 　杨九光, 龙村, 孙立忠, 等．全主动脉弓置换术中的温度管理．中国胸心血管外科临床杂志, 2005,12(5)：312-315.
5. 　田良鑫, 孙立忠, 程卫平, 等. 单侧与双侧顺行性脑灌注对认知能力的影响. 中国胸心血管外科临床杂志, 2005,12(1)：8-10.
6. 　Joachimsson PO, Sjöberg F, Forsman M, et al．Adverse effects of hyperoxemia during cardiopulmonary bypass．J Thorac Cardiovasc Surg, 1996, 112(3)：812-819.
7. 　Dexter F, Kern FH, Hindman BJ, et al．The brain uses mostly dissolved oxygen during profoundly hypothermic cardiopulmonary bypass. Ann Thorac Surg, 1997, 63(6)：1725-1729.
8. 　Nollert G, Nagashima M, Bucerius J,et al．Oxygenation strategy and neurologic damage after deep hypothermic circulatory arrest. Ⅰ.Gaseous microemboli. J Thorac Cardiovasc Surg, 1999,117(6)：1166-1171.
9. 　Leyvi G, Bello R, Wasnick JD, et al．Assessment of cerebral oxygen balance during deep hypothermic circulatory arrest by continuous jugular bulb venous saturation and near-infrared spectroscopy. J Cardiothorac Vasc Anesth, 2006, 20(6)：826-833.
10. 　Cormio M, Valadka AB, Robertson CS．Elevated jugular venous oxygen saturation after severe head injury．J Neurosurg , 1999, 90(1)：9-15．.
11. 　Croughwell ND, Newman MF, Blumenthal JA, et al．Jugular bulb saturation and cognitive dysfunction after cardiopulmonary bypass. Ann Thorac Surg,1994, 58(6)：1702-1708.
12. 　Young C，Tenkova T, Dikranian k，et a1．Excitotoxic versus apoptotic mechanisms of neuronal cell death in perinatal hypoxia／ischemia．Curr Mol Med，2004, 4(2)：77-85．.
13. 　Liu Y, Rosenthal RE, Haywood Y, et al．Normoxic ventilation after cardiac arrest reduces oxidation of brain lipids and improves neurological outcome. Stroke, 1998, 29(8)：1679-1686.
14. 　Kilgannon JH, Jones AE, Shapiro NI, et al．Association between arterial hyperoxia following resuscitation from cardiac arrest and inhospital mortality. JAMA, 2010, 303(21)：2165-2171.
15. 　McCord JM, Fridovich I．Superoxide dismutase. J Biol Chem, 1969, 244(22)：6049-6055.
16. 　Lewén A, Matz P, Chan PH．Free radical pathways in CNS injury. J Neurotrauma, 2000, l7(10)：871-890.
17. 　Kamada H, Yu F, Nito C, et al．Influence of hyperglycemia on oxidative stress and matrix metalloproteinase-9 activation after focal cerebral ischemia/reperfusion in rats：relation to blood-brain barrier dysfunction. Stroke, 2007,38(3)：1044-1049.
18. 　Maier CM, Hsieh L, Crandall T, et al．Evaluating therapeutic targets for reperfusion-related brain hemorrhage. Ann Neurol, 2006, 59(6)： 929-938.
19. 　Narasimhan P, Liu J, Song YS, et al．VEGF stimulates the ERK 1/2 signaling pathway and apoptosis in cerebral endothelial cells after ischemic conditions. Stroke, 2009, 40(4)： 1467-1473.
20. 　祝忠群, 朱德明, 苏肇伉, 等．先天性心脏病儿体外循环的再氧合损伤．中国体外循环杂志, 2005,3(3)：131-133.
21. 　Pearl JM, Thomas DW, Grist G, et al．Hyperoxia for management of acid-base status during deep hypothermia with circulatory arrest. Ann Thorac Surg, 2000，70(3)：751-755.

Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Hyperoxia Management During Deep Hypothermia for Cerebral Protection in a Circulatory Arrest Rabbit Model

Abstract Full text Figures/Tables Video References Cited by

Format

Content