Mild postischemic hypothermia limits cerebral injury following transient focal ischemia in rat neocortex.
Mild postischemic hypothermia limits cerebral injury following transient focal ischemia in rat neocortex.
复制标题
轻度缺血后低温可限制大鼠新皮质短暂局灶性缺血后的脑损伤。
DOI：
10.1016/0006-8993(96)00122-9
复制
发表时间：
1996
期刊：
影响因子：
2.9
通讯作者：
Lee,KS
中科院分区：
文献类型：
--
作者：
Yanamoto,H;Hong,SC;Soleau,S;Kassell,NF;Lee,KS
缺血内亚低温已被证明可以减轻短暂局灶性缺血后发生的脑梗死。相比之下，轻度低温在缺血后给药时提供保护作用的能力尚未明确定义为短暂的局灶性事件，如发生在许多类型的中风。本研究探讨了这个问题，通过调查的时间和持续时间的影响，亚低温对脑梗死的大鼠模型的可逆性局灶性缺血。Sprague-Dawley大鼠（n = 45）进行3小时的局灶性新皮质缺血可逆闭塞大脑中动脉和两个颈动脉。再灌注后建立轻度低温，并维持短暂（1小时）或延长（21小时）。缺血后24或48 h处死动物。一个显着减少（32%）的梗死体积时，再灌注后立即建立低温，并保持了较长的时间（21小时）。相比之下，立即但短暂（1小时）的低温并没有减少梗死体积。将低温延迟至再灌注后30分钟并维持21小时可使梗死体积减少22%;然而，这种效果并未达到统计学显著性。这些研究结果表明，轻度缺血后低温能够保护脑损伤后短暂局灶性缺血，但需要延长低温达到这一效果。这些发现与越来越多的证据一致，即短暂性局灶性缺血后的治疗机会窗口相当短暂，并且这种形式的缺血性损伤中涉及的关键机制在相当长的缺血后间隔内保持激活。
Intraischemic mild hypothermia has been shown to attenuate cerebral infarction occurring after transient focal ischemia. In contrast, the capacity of mild hypothermia to provide a protective effect when administered postischemically has not been clearly defined for transient focal events such as occur in many types of stroke. The present study addressed this issue by investigating the influence of timing and duration of mild hypothermia on cerebral infarction in a rat model of reversible focal ischemia. Sprague-Dawley rats (n = 45) were subjected to 3 h of focal neocortical ischemia by occluding reversibly one middle cerebral artery and both carotid arteries. Mild hypothermia was established after reperfusion and maintained for brief (1 h) or prolonged (21 h) periods. Animals were sacrificed 24 or 48 h after ischemia. A significant reduction (32%) in the volume of infarction was obtained when hypothermia was established immediately after reperfusion and maintained for a prolonged (21 h) period. In contrast, immediate but brief (1 h) hypothermia did not reduce infarction volume. Delaying hypothermia until 30 min post reperfusion and maintaining it for 21 h reduced infarction volume by 22%; however, this effect did not achieve statistical significance. These findings demonstrate that mild postischemic hypothermia is capable of protecting against cerebral injury following transient focal ischemia but that prolonged hypothermia is required to achieve this effect. These findings are consistent with increasing evidence that the window of therapeutic opportunity after transient focal ischemia is rather brief and that critical mechanisms involved in this form of ischemic injury remain activated over a rather lengthy postischemic interval.