Histochemical and electron microscopic study on motor neurone degeneration following transient spinal cord ischaemia at normothermic conditions in rabbits

被引:9
作者
Lee, JC
Hwang, IK
Park, SK
Yoo, KY
Seo, K
Kang, TC
Oh, YS
Won, MH [1 ]
机构
[1] Hallym Univ, Coll Med, Dept Anat, Chunchon 200702, South Korea
[2] Ewha Womans Univ, Ewha Inst Neurosci, Ewha Med Sch, Dept Pharmacol, Seoul 110783, South Korea
[3] Seoul Natl Univ, Coll Vet Med, Dept Vet Surg, Seoul 151742, South Korea
[4] Hallym Univ, Coll Med, Med Genet & Expt Anim Ctr, Chunchon 200702, South Korea
关键词
D O I
10.1111/j.1439-0264.2005.00603.x
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
This study was carried out to investigate the motor neurone degeneration in the ventral horn following transient spinal cord ischaemia at normothermic conditions in rabbits. Transient spinal cord ischaemia was induced by occlusion of the abdominal aorta underneath the left renal artery for 15 min at normothermia (38.7 degrees C). Sections at the level of L7 were examined using histochemical and electron microscopic methods. Cresyl violet-positive motor neurones began to reduce in number at 3 h after ischaemia reperfusion, and were not detectable at 48 h after ischaemia reperfusion. Acid fuchsin-positive motor neurones were detected at 1 h after ischaemia reperfusion, significantly increased up to 6 h after the ischaemia reperfusion, and eventually disappeared by 48 h after ischaemia reperfusion. In electron microscopic findings, the disintegration of cytoplasmic membranes, and the disruption of mitochondria and endoplasmic reticulum were observed in motor neurones at 30 min after ischaemia reperfusion. Motor neurones showed necrotic findings with pyknotic degeneration at 1 h after ischaemia reperfusion. The necrotic degeneration became severer time dependently after ischaemia reperfusion. At 48 h after ischaemia reperfusion, cellular components were not detectable in motor neurones. In conclusion, we suggest that the degeneration pattern of motor neurones of the ischaemic spinal cord was necrotic after ischaemia reperfusion under normothermic conditions.
引用
收藏
页码:252 / 257
页数:6
相关论文
共 31 条
[1]   PROTECTION AGAINST HIPPOCAMPAL CA1 CELL LOSS BY POSTISCHEMIC HYPOTHERMIA IS DEPENDENT ON DELAY OF INITIATION AND DURATION [J].
CARROLL, M ;
BEEK, O .
METABOLIC BRAIN DISEASE, 1992, 7 (01) :45-50
[2]   NEUROLOGICAL OUTCOME CORRELATED WITH SPINAL EVOKED-POTENTIALS IN A SPINAL-CORD ISCHEMIA MODEL [J].
CHENG, MK ;
ROBERTSON, C ;
GROSSMAN, RG ;
FOLTZ, R ;
WILLIAMS, V .
JOURNAL OF NEUROSURGERY, 1984, 60 (04) :786-795
[3]   DELAYED AND PROLONGED POSTISCHEMIC HYPOTHERMIA IS NEUROPROTECTIVE IN THE GERBIL [J].
COLBOURNE, F ;
CORBETT, D .
BRAIN RESEARCH, 1994, 654 (02) :265-272
[4]   PROGRESS IN TREATMENT OF THORACOABDOMINAL AND ABDOMINAL AORTIC-ANEURYSMS INVOLVING CELIAC, SUPERIOR MESENTERIC, AND RENAL-ARTERIES [J].
CRAWFORD, ES ;
SNYDER, DM ;
CHO, GC ;
ROEHM, JOF .
ANNALS OF SURGERY, 1978, 188 (03) :404-422
[5]   NEUROPATHOLOGY OF EXPERIMENTAL SPINAL-CORD ISCHEMIA IN THE RABBIT [J].
DEGIROLAMI, U ;
ZIVIN, JA .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1982, 41 (02) :129-149
[6]  
FOSBURG RG, 1976, INJURIES SPINE SPI 2, P63
[7]   Apoptosis of motor neurons with induction of caspases in the spinal cord after ischemia [J].
Hayashi, T ;
Sakurai, M ;
Abe, K ;
Sadahiro, M ;
Tabayashi, K ;
Itoyama, Y .
STROKE, 1998, 29 (05) :1007-1012
[8]   RISK OF SPINAL-CORD DYSFUNCTION IN PATIENTS UNDERGOING THORACOABDOMINAL AORTIC REPLACEMENT [J].
HOLLIER, LH ;
MONEY, SR ;
NASLUND, TC ;
PROCTER, CD ;
BUHRMAN, WC ;
MARINO, RJ ;
HARMON, DE ;
KAZMIER, FJ ;
ASCER, E ;
BAKER, JD ;
CHERRY, KJ ;
COHEN, JR .
AMERICAN JOURNAL OF SURGERY, 1992, 164 (03) :210-214
[9]   Chronological alterations of calbindin D-28k immunoreactivity in the gerbil main olfactory bulb after ischemic insult [J].
Hwang, IK ;
Kang, TC ;
Lee, JC ;
Park, SK ;
An, SJ ;
Lee, IS ;
Lee, YB ;
Sohn, HS ;
Kang, JH ;
Choi, SY ;
Won, MH .
BRAIN RESEARCH, 2003, 971 (02) :250-254
[10]   BLOOD-FLOW AND VASCULAR-PERMEABILITY DURING MOTOR DYSFUNCTION IN A RABBIT MODEL OF SPINAL-CORD ISCHEMIA [J].
JACOBS, TP ;
KEMPSKI, O ;
MCKINLEY, D ;
DUTKA, AJ ;
HALLENBECK, JM ;
FEUERSTEIN, G .
STROKE, 1992, 23 (03) :367-373