Marion D W, Leonov Y, Ginsberg M, Katz L M, Kochanek P M, Lechleuthner A, Nemoto E M, Obrist W, Safar P, Sterz F, Tisherman S A, White R J, Xiao F, Zar H
Department of Neurological Surgery, Presbyterian University Hospital, University of Pittsburgh Medical Center, PA 15213, USA.
Crit Care Med. 1996 Feb;24(2 Suppl):S81-9.
Resuscitative (postinsult) hypothermia is less well studied than protective-preservative (pre- and intra-arrest) hypothermia. The latter is in wide clinical use, particularly for protecting the brain during cardiac surgery. Resuscitative hypothermia was explored in the 1950s and then lay dormant until the 1980s when it was revived. This change occurred through the discoveries of brain damage mitigating effects after cardiac arrest in dogs, and after forebrain ischemia in rats, of mild (34 degrees C) hypothermia (which is safe), and of benefits derived from moderate hypothermia (30 degrees C) after traumatic brain injury or focal brain ischemia in various species. The idea that protection-preservation or resuscitation by hypothermia is mainly explained by its ability to reduce cerebral oxygen demand has been replaced by an increasingly documented synergism of many beneficial mechanisms. Deleterious chemical cascades during and after these insults are suppressed even by mild hypothermia. Prolonged moderate hypothermia carries some risks, e.g., arrhythmias, infection and coagulopathies. These side effects need further study. In global brain ischemia, protective-preservative mild hypothermia provides lasting mitigation of brain damage. Resuscitative mild hypothermia, however, may be beneficial in terms of long-term outcome or may merely delay the inevitable loss of selectively vulnerable neurons. Even if the latter is true, mild hypothermia may extend the therapeutic window for other interventions. This extension of the therapeutic window requires further documentation. After normothermic cardiac arrest of 11 mins in dogs, mild resuscitative hypothermia from 15 mins to 12 hours after reperfusion plus cerebral blood flow promotion normalized functional recovery with the least histologic damage seen thus far. Optimal duration of, and rewarming methods from, resuscitative hypothermia need clarification. The earliest possible induction of mild hypothermia after cardiac arrest seems desirable. Head-neck surface cooling alone is too slow. Among many clinically feasible rapid cooling methods, carotid cold flush and peritoneal cooling look promising. After traumatic brain injury or focal brain ischemia, which seem to still benefit from even later cooling, surface cooling methods may be adequate. Resuscitative hypothermia after cardiac arrest, traumatic brain injury, or focal brain ischemia should be considered for clinical trials.
复苏性（损伤后）低温疗法的研究不如保护性 - 预防性（心脏骤停前和骤停期间）低温疗法充分。后者在临床中广泛应用，尤其是在心脏手术期间用于保护大脑。复苏性低温疗法在20世纪50年代曾被探索，之后沉寂直至80年代才重新兴起。这种变化源于多项发现，包括犬心脏骤停后、大鼠前脑缺血后轻度（34摄氏度）低温（安全）对脑损伤的减轻作用，以及不同物种在创伤性脑损伤或局灶性脑缺血后中度低温（30摄氏度）的益处。低温用于保护 - 预防或复苏主要是通过降低脑氧需求这一观点，已被越来越多记录在案的多种有益机制的协同作用所取代。即使是轻度低温也能抑制这些损伤期间及之后有害的化学级联反应。长时间的中度低温存在一些风险，如心律失常、感染和凝血功能障碍。这些副作用需要进一步研究。在全脑缺血中，保护性 - 预防性轻度低温可持久减轻脑损伤。然而，复苏性轻度低温在长期预后方面可能有益，或者可能仅仅延迟选择性易损神经元不可避免的损失。即便后者属实，轻度低温也可能延长其他干预措施的治疗窗。这种治疗窗的延长需要进一步论证。犬在常温下心脏骤停11分钟后，再灌注后15分钟至12小时进行轻度复苏性低温并促进脑血流，可使功能恢复正常，且组织学损伤是目前所见最小的。复苏性低温的最佳持续时间及复温方法需要明确。心脏骤停后尽早诱导轻度低温似乎是可取的。仅头部 - 颈部表面降温太慢。在许多临床可行的快速降温方法中，颈动脉冷冲洗和腹膜降温看起来很有前景。在创伤性脑损伤或局灶性脑缺血后，即使更晚进行降温似乎仍有益处，表面降温方法可能就足够了。心脏骤停、创伤性脑损伤或局灶性脑缺血后的复苏性低温疗法应考虑用于临床试验。
