Xia Xiao-yan, Xia Yi-xin
Department of Obstetrics, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100026, China.
Chin Med Sci J. 2011 Mar;26(1):49-53. doi: 10.1016/s1001-9294(11)60019-9.
To investigate the effect of graded hypothermia on neuropathologic alterations of neonatal rat brain after exposed to hypoxic-ischemic insult at 37°C, 33°C, 31°C, and 28°C, respectively, and to observe the effect of hypothermia on 72-kDa heat shock protein (HSP72) expression after hypoxic-ischemic insult.
Seven days old Wistar rats were subjected to unilateral common carotid artery ligation followed by exposure to hypoxia in 8% oxygen for 2 hours at 37°C, 33°C, 31°C, and 28°C, respectively. The brain temperature was monitored indirectly by inserting a mini-thermocouple probe into the temporal muscle during hypoxia. After hypoxia-ischemia their mortality was assessed. Neuronal damage was assessed with HE staining 72 hours after hypoxia. HSP72 expression at 0.5, 24, and 72 hours of recovery was immunohistochemically assessed using a monoclonal antibody to HSP72.
Hypoxia-ischemia caused 10.5% (2/19) of mortality in rat of 37°C group, but no death occurred in 33°C, 31°C or 28°C groups. HE staining showed neuropathologic damage was extensive in rats exposed to hypoxia-ischemia at 37°C (more than 80.0%). The incidence of severe brain damage was significantly decreased in 33°C (53.3%) and 31°C groups (44.4%), and no histologic injury was seen in the 28°C group of rats. Expression of HSP72 was manifest and persistent in the rat brain of 37°C group, but minimum in the rat brain of 28°C group.
Mild and moderate hypothermia might prevent cerebral visible neuropathologic damage associated with hypoxic-ischemic injury by decreasing stress response.
分别研究37℃、33℃、31℃和28℃的分级低温对新生大鼠脑在37℃暴露于缺氧缺血性损伤后的神经病理改变的影响，并观察低温对缺氧缺血性损伤后72-kDa热休克蛋白（HSP72）表达的影响。
7日龄Wistar大鼠分别接受单侧颈总动脉结扎，随后分别在37℃、33℃、31℃和28℃暴露于8%氧气的低氧环境2小时。在低氧期间通过将微型热电偶探头插入颞肌间接监测脑温。缺氧缺血后评估其死亡率。缺氧72小时后用HE染色评估神经元损伤。使用抗HSP72单克隆抗体免疫组化评估恢复0.5、24和72小时时的HSP72表达。
37℃组大鼠缺氧缺血导致10.5%（2/19）死亡，但33℃、31℃或28℃组未发生死亡。HE染色显示，37℃暴露于缺氧缺血的大鼠神经病理损伤广泛（超过80.0%）。33℃组（53.3%）和31℃组（44.4%）严重脑损伤的发生率显著降低，28℃组大鼠未见组织学损伤。HSP72在37℃组大鼠脑中表达明显且持续，但在28℃组大鼠脑中最低。
轻度和中度低温可能通过降低应激反应预防与缺氧缺血性损伤相关的脑可见神经病理损伤。
