Török Elisabeth, Klopotowski Mariusz, Trabold Raimund, Thal Serge C, Plesnila Nikolaus, Schöller Karsten
Institute for Surgical Research, University of Munich Medical Center, Grosshadern, Ludwig-Maximilians University, Munich, Germany.
Neurosurgery. 2009 Aug;65(2):352-9; discussion 359. doi: 10.1227/01.NEU.0000345632.09882.FF.
After a subarachnoid hemorrhage (SAH), the primary cause of mortality is secondary brain injury occurring within the first 48 hours after the initial bleeding. Because of the unknown pathophysiology of these early events, therapeutic approaches are scarce. Because mild hypothermia (33 degrees C) is among the strongest neuroprotectants known so far, the aim of this study was to investigate acute and delayed effects of hypothermia if applied after SAH.
Male Sprague-Dawley rats were subjected to SAH and randomly assigned to the following groups: 1) SAH under normothermia, 2) SAH followed by 2 hours of hypothermia starting 1 hour after the bleeding, and 3) SAH followed by 2 hours of hypothermia starting 3 hours after the bleeding. Cerebral blood flow and intracranial pressure were continuously measured up to 6 hours after SAH. Mortality, neurological deficits, and body weight were assessed from postoperative day 1 to day 7. Brain water content and morphological brain damage were quantified 24 hours and 7 days after SAH, respectively.
Mild hypothermia reduced intracranial pressure (P < 0.001) and posthemorrhagic neurological deficits (P < 0.05) and improved postoperative weight gain significantly (P < 0.05). Mortality, cerebral blood flow, and the formation of cerebral edema were not significantly influenced by mild hypothermia.
The current results show that mild hypothermia (33 degrees C) exhibits sustained neuroprotection if applied up to 3 hours after SAH. Overall, mild hypothermia seems to be an effective neuroprotective strategy after SAH and should therefore be evaluated as a treatment option for SAH in patients.
蛛网膜下腔出血(SAH)后,死亡的主要原因是初次出血后48小时内发生的继发性脑损伤。由于这些早期事件的病理生理学尚不清楚,治疗方法很少。由于轻度低温(33摄氏度)是目前已知最强的神经保护剂之一,本研究的目的是探讨SAH后应用低温的急性和延迟效应。
雄性Sprague-Dawley大鼠接受SAH,并随机分为以下几组:1)常温下的SAH;2)出血后1小时开始进行2小时低温治疗的SAH;3)出血后3小时开始进行2小时低温治疗的SAH。SAH后持续测量脑血流量和颅内压6小时。从术后第1天至第7天评估死亡率、神经功能缺损和体重。分别在SAH后24小时和7天对脑含水量和脑形态损伤进行量化。
轻度低温降低了颅内压(P<0.001)和出血后神经功能缺损(P<0.05),并显著改善了术后体重增加(P<0.05)。轻度低温对死亡率、脑血流量和脑水肿的形成没有显著影响。
目前的结果表明,SAH后3小时内应用轻度低温(33摄氏度)具有持续的神经保护作用。总体而言,轻度低温似乎是SAH后一种有效的神经保护策略,因此应作为SAH患者的一种治疗选择进行评估。