Resuscitative hypothermia.
Resuscitative hypothermia.
复制标题
复苏性低温。
作者：
D. Marion;Y. Leonov;M. Ginsberg;L. Katz;P. Kochanek;A. Lechleuthner;E. Nemoto;W. Obrist;P. Safar;F. Sterz;S. Tisherman;R. White;F. Xiao;H. Zar
复苏性（损伤后）低温比保护性-防腐性（前和内逮捕）低温研究较少。后者在临床上应用广泛，特别是在心脏手术期间用于保护大脑。复苏性低温在20世纪50年代被探索，然后一直处于休眠状态，直到20世纪80年代才恢复。这一变化是通过发现犬心脏骤停后和大鼠前脑缺血后的脑损伤减轻作用，轻度（34 ℃）低温（这是安全的），以及各种物种创伤性脑损伤或局灶性脑缺血后中度低温（30 ℃）的益处而发生的。低温的保护-保存或复苏主要是通过其降低脑需氧量的能力来解释的观点已经被越来越多的证据证明的许多有益机制的协同作用所取代。在这些伤害过程中和之后，有害的化学级联反应甚至被轻度低温抑制。长期中度低温会带来一些风险，例如，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-防腐性亚低温可持久减轻脑损伤。然而，复苏性轻度低温可能对长期结果有利，或者可能只是推迟选择性脆弱神经元的不可避免的丧失。即使后者是真的，轻度低温也可能延长其他干预措施的治疗窗口。这种治疗窗的扩展需要进一步的文件。犬常温心脏停搏11分钟后，再灌注后15分钟至12小时的轻度复苏低温加上脑血流促进使功能恢复正常，迄今为止观察到的组织学损伤最小。复苏性低温的最佳持续时间和复温方法需要澄清。心脏骤停后尽早诱导轻度低温似乎是可取的。头颈部表面单独冷却太慢。在许多临床上可行的快速冷却方法中，颈动脉冷冲洗和腹膜冷却看起来很有前途。在创伤性脑损伤或局灶性脑缺血后，表面冷却方法可能就足够了，这些似乎仍然受益于更晚的冷却。心脏骤停、创伤性脑损伤或局灶性脑缺血后的复苏性低温应考虑用于临床试验。
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or resuscitation by hypothermia is mainly explained by its ability to reduce cerebral oxygen demand has been replaced by an increasingly documented synergism of many beneficial mechanisms.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.