Cell proliferation and death of growth plate chondrocyte caused by ischemia and reperfusion.
Microsurgery
; 21(1): 30-6, 2001.
Article
em En
| MEDLINE
| ID: mdl-11426638
ABSTRACT
The aim of this study was to assess the short-term response of cell kinetics of growth plate chondrocytes under conditions of warm ischemia and reperfusion. To understand the time-course changes that occur after reperfusion, 0 and 6 h of warm ischemia was produced in the right hindlimb of 35-day-old Wistar rats by isolating the vascular pedicle occlusion. The animals were killed at 12, 24, 48, or 96 h postoperatively after reperfusion, and proximal tibia growth plates were investigated. To investigate the effect of the ischemia period on the kinetics of growth plate chondrocytes, 0, 2, 4, 6, and 8 h of ischemia was induced, and the animals were killed for evaluation 24 h after reperfusion. For evaluation of cell kinetics, BrdU was used to observe the changes in cell proliferation of growth plate chondrocytes, and TUNEL was used to estimate the changes in rate of cell death. In the time-course study, both 0 and 6 h of ischemia increased cell proliferation at 12 and 24 h after reperfusion; however, at 48 and 96 h, the proliferation rate was not further increased. At 12 and 24 h postoperatively, 6 h of ischemia increased chondrocyte proliferation more than 0 h of ischemia with significant differences; 6 h of ischemia led to an increased cell death rate at 12, 24, and 48 h postoperatively, whereas 0 h of ischemia did not affect the cell death rate. In the ischemia time-dependent study, the cell proliferation rate induced by 4 h of ischemia was highest in all controlled periods of ischemia. Cell death rate increased gradually with increases in ischemia time 24 h after reperfusion. This experiment showed that ischemic damage causes short-term postoperative changes in the kinetics of growth plate chondrocytes.
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Base de dados:
MEDLINE
Assunto principal:
Tíbia
/
Condrócitos
/
Lâmina de Crescimento
/
Isquemia
Idioma:
En
Ano de publicação:
2001
Tipo de documento:
Article