Evaluation of rapid ischemic preconditioning in a rabbit model of spinal cord ischemia

被引:45
作者
Kakimoto, M
Kawaguchi, M
Sakamoto, T
Inoue, S
Furuya, H
Nakamura, M
Konishi, N
机构
[1] Nara Med Univ, Dept Anesthesiol, Kashihara, Nara 6348522, Japan
[2] Nara Med Univ, Dept Pathol, Kashihara, Nara 6348522, Japan
关键词
D O I
10.1097/00000542-200311000-00017
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background: Rapid ischemic preconditioning (IPC) has been shown to reduce cellular injury after subsequent cardiac and cerebral ischemia. However, the data on rapid IPC of the spinal cord is limited. The authors investigated whether pretreatment with sublethal ischemia of spinal cord can attenuate neuronal injury after spinal cord ischemia in rabbits. Methods: Forty-seven male New Zealand white rabbits were randomly assigned to one of three groups (n = 15 or 16 each). In the IPC(-) group, the infrarenal aorta was occluded for 17 min to produce spinal cord ischemia. In the IPC(+) group, 5 min of aortic occlusion was performed 30 min before 17 min of spinal cord ischemia. in the sham group, the aorta was not occluded. Hind limb motor function was assessed at 3 h, 24 h, 4 days, and 7 days after reperfusion using Tarlov scoring (0 = paraplegia; 4 = normal). Animals were killed for histopathologic evaluation at 24 h or 7 days after reperfusion. The number of normal neurons in the anterior spinal cord (L4-L6) was counted. Results: Neurologic scores were significantly higher in the IPC(+) group than the IPC(-) group at 3 and 24 h after reperfusion (P < 0.05). However, neurologic scores in the IPC(+) group gradually decreased and became similar to those in the IPC(-) group at 4 and 7 days after reperfusion. At 24 h after reperfusion, the numbers of normal neurons were significantly higher in the IPC (+) group than in the IPC(-) group (P < 0.05) and were similar between the IPC(+) and sham groups. At 7 days after reperfusion, there was no difference in the number of normal neurons between the IPC(+) and IPC(-) groups. Conclusion: The results indicate that rapid IPC protects the spinal cord against neuronal damage 24 h but not 7 days after reperfusion in a rabbit model of spinal cord ischemia, suggesting that the efficacy of rapid IPC may be transient.
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页码:1112 / 1117
页数:6
相关论文
共 17 条
[1]   Pharmacological preconditioning ameliorates neurological injury in a model of spinal cord ischemia [J].
Caparrelli, DJ ;
Cattaneo, SM ;
Bethea, BT ;
Shake, JG ;
Eberhart, C ;
Blue, ME ;
Marbán, E ;
Johnston, MV ;
Baumgartner, WA ;
Gott, VL .
ANNALS OF THORACIC SURGERY, 2002, 74 (03) :838-844
[2]   Ischemic preconditioning:: From adenosine receptor to KATP channel [J].
Cohen, MV ;
Baines, CP ;
Downey, JM .
ANNUAL REVIEW OF PHYSIOLOGY, 2000, 62 :79-109
[3]   Morbidity and mortality after extent II thoracoabdominal aortic aneurysm repair [J].
Coselli, JS ;
LeMaire, SA ;
Conklin, LD ;
Köksoy, C ;
Schmittling, ZC .
ANNALS OF THORACIC SURGERY, 2002, 73 (04) :1107-1115
[4]   The outcome in the United States after thoracoabdominal aortic aneurysm repair, renal artery bypass, and mesenteric revascularization [J].
Derrow, AE ;
Seeger, JM ;
Dame, DA ;
Carter, RL ;
Ozaki, CK ;
Flynn, TC ;
Huber, TS .
JOURNAL OF VASCULAR SURGERY, 2001, 34 (01) :54-60
[5]   Experimental study of the protection of ischemic preconditioning to spinal cord ischemia [J].
Fan, T ;
Wang, CC ;
Wang, FM ;
Cheng, F ;
Qiao, H ;
Liu, SL ;
Guo, W ;
Xiang, FY .
SURGICAL NEUROLOGY, 1999, 52 (03) :299-305
[6]   TEMPORAL PROFILE OF THE EFFECTS OF PRETREATMENT WITH BRIEF CEREBRAL-ISCHEMIA ON THE NEURONAL DAMAGE FOLLOWING SECONDARY ISCHEMIC INSULT IN THE GERBIL - CUMULATIVE DAMAGE AND PROTECTIVE EFFECTS [J].
KATO, H ;
LIU, Y ;
ARAKI, T ;
KOGURE, K .
BRAIN RESEARCH, 1991, 553 (02) :238-242
[7]   Ischemic tolerance [J].
Kirino, T .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2002, 22 (11) :1283-1296
[8]   PRECONDITIONING WITH ISCHEMIA - A DELAY OF LETHAL CELL INJURY IN ISCHEMIC MYOCARDIUM [J].
MURRY, CE ;
JENNINGS, RB ;
REIMER, KA .
CIRCULATION, 1986, 74 (05) :1124-1136
[9]   Rapid tolerance to focal cerebral ischemia in rats is attenuated by adenosine A1 receptor antagonist [J].
Nakamura, M ;
Nakakimura, K ;
Matsumoto, M ;
Sakabe, T .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2002, 22 (02) :161-170
[10]   The effect of rapid preconditioning on the microglial, astrocytic and neuronal consequences of global cerebral ischemia [J].
Pérez-Pinzón, MA ;
Vitro, TM ;
Dietrich, WD ;
Sick, TJ .
ACTA NEUROPATHOLOGICA, 1999, 97 (05) :495-501