PROTECTIVE EFFECT OF MILD HYPOTHERMIA
ON HYPOXIA-ISCHEMIC BRAIN DAMAGE
Jiang Chunming, Mi Yan
The First Hospital of Harbin Medical
University, Harbin, China
Objectives: The aim of this study is to examine the
protective effect of mild hypothermia on hypoxia-ischemic brain damage
(HIBD) in the neonate and to define the optimal therapeutic window of
hypothermia.
Methods: The HIBD model was produced in the traditional
model of neonatal hypoxia-ischemic (HI) which subjected 7-old-day Wistar
rats to unilateral carotid artery ligation followed by an hypoxic (8%
oxyger) episode of 2 hours duration. The rats were divided into five groups
randomly. Group��: sham-operated. Group��:No treatment was applied to animal after hypoxic-ischemic onset.
Group ��:4 hours of hypothermia was applied to animal at
30 minutes after the hypoxic-ischemic onset. Group ��:hypothermia was applied at 1 hours after hypoxic-ischemic onset.
Group ��:hypothermia was applied at 3 hours after the
hypoxic-ischemic onset. The homogenate of cortical cells was used to
determine malonyldialdehyde (MDA) content and superoxide dismutase (SOD)
activities. Apoptosis neuronal cell was observed by terminal
deoxynucleotidyl transferase mediated dUTP-biotin nick end labelling(TUNEL)
staining and bax gene expressing.
Results: The MDA content was 170.25 �� 17.00; 325.78 ��
10.77; 244.02 �� 17.07; 298.95 �� 14.74; 312.22 �� 14.57 (mean �� standard
error of the mean, n = 15 per group) for ��.��.��.��.��groups
respectively. The SOD activities for these five respective groups were
31.69��3.30; 51.23��3.10; 60.63��3.38; 53.47��2.45; 52.22��1.91 (mean �� standard
error of the mean,n = 15 per group). The MDA content of group �� was significantly lower than group��.��.��(p<0.01). The number of apoptosis cell for ��.��.��groups was 18.80��1.37; 15.53��0.64; 19.53��0.92
(mean��standard error of the mean,n = 15 per group). The number of the cell
that expressed bax gene was 35.87��1.64; 29.13��1.81;
36.20��1.47(mean��standard error of the mean, n = 15 per group). Contrast
with group��,apoptosis cell of group �� was significantly lower(p<0.01), but group �� has no difference with group ��,moreover the apoptosis cell of group �� was higher than group �� obviously(p<0.01).
Conclusions :These results demonstrated that hypothermia prevented
hypoxic-ischemic brain damage by suppressing the generation of free
radicals and the apoptosis of cells; the optimal therapeutic window of mild
hypothermia was within the 30 minutes after the onset of hypoxic-ischemic.