The aim of this study was to assess the short-term response of cell kinetic
s of growth plate chondrocytes under conditions of warm ischemia and reperf
usion. To understand the timecourse 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 k
illed at 12, 24, 48, or 96 h postoperatively after reperfusion, and proxima
l tibia growth plates were investigated. To investigate the effect of the i
schemia period on the kinetics of growth plate chondrocytes, 0, 2, 4, 6, an
d 8 h of ischemia was induced, and the animals were killed for evaluation 2
4 h after reperfusion. For evaluation of cell kinetics, BrdU was used to ob
serve the changes in cell proliferation of growth plate chondrocytes, and T
UNEL was used to estimate the changes in rate of cell death. In the time-co
urse study, both 6 and 6 h of ischemia increased cell proliferation at 12 a
nd 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 signific
ant differences; 6 h of ischemia led to an increased cell death rate at 12,
24, and 48 h postoperatively, whereas 6 h of ischemia did not affect the c
ell death rate. In the ischemia time-dependent study, the cell proliferatio
n rate induced by 4 h of ischemia was highest in all controlled periods of
ischemia. Cell death rate increased gradually with increases in ischemia ti
me 24 h after reperfusion. This experiment showed that ischemic damage caus
es short-term postoperative changes in the kinetics of growth plate chondro
cytes. (C) 2001 Wiley-Liss, Inc.