The time course of acquisition of ischemic tolerance and induction of heatshock protein 70 after a brief period of ischemia in the spinal cord in rabbits

Citation
M. Matsumoto et al., The time course of acquisition of ischemic tolerance and induction of heatshock protein 70 after a brief period of ischemia in the spinal cord in rabbits, ANESTH ANAL, 92(2), 2001, pp. 418-423
Citations number
13
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIA AND ANALGESIA
ISSN journal
00032999 → ACNP
Volume
92
Issue
2
Year of publication
2001
Pages
418 - 423
Database
ISI
SICI code
0003-2999(200102)92:2<418:TTCOAO>2.0.ZU;2-#
Abstract
We examined the time course of development of ischemic tolerance in the spi nal cord and sought its mechanism exploring the expression of heat shock pr otein 70 (HSP70). Spinal cord ischemia was produced in rabbits by occlusion of the abdominal aorta. In Experiment 1, neurologic and histopathologic ou tcome was evaluated 48 h after prolonged ischemia (20 min) that was given 2 days, 4 days, or 7 days after a short period of ischemia (ischemic pretrea tment) sufficient to abolish postsynaptic component of spinal cord evoked p otentials. Control animals were given prolonged ischemia 4 days after sham operation. In Experiment 2, HSP70 expression in motor neurons after pretrea tment without exposure to prolonged ischemia was examined by immunohistoche mical staining. Ischemic pretreatment 4 days (but not 2 days or 7 days) bef ore 20 min ischemia exhibited protective effects against spinal cord injury . In the cytoplasm,HSP70 immunoreactivity was mildly increased after 2, 4,a nd 7 days of ischemic pretreatment. However, the incidence of nuclear HSP70 immunoreactivity 2 days, 4 days, and 7 days after ischemic pretreatment wa s 2 of 6 animals, 4 of 6 animals, and 1 of 6 animals, respectively (none in the control group). These results suggest that ischemic tolerance is appar ent 4 days after ischemic pretreatment and that HSP70 immunoreactivity in t he nucleus may provide some insight into the mechanisms of ischemic toleran ce in the spinal cord.