Safar P, Stezoski W, Nemoto E M
Arch Neurol. 1976 Feb;33(2):91-5. doi: 10.1001/archneur.1976.00500020019004.
To determine the efficacy of cerebral microcirculation promoting therapy in postischemic brain failure, 11 dogs awakening from methohexital sodium anesthesia were subjected to 12 minutes of reversible circulatory arrest by ventricular fibrillation. Physiological variables were controlled for six hours after resuscitation, and the dogs were observed for seven days. Six dogs without the special postresuscitative therapy did not awaken, and either died within 36 hours or remained comatose for seven days. In five dogs, a combination of the following measures was applied: (1) mean arterial pressure was raised to 150 to 180 mm Hg with norepinephrine for six hours; (2) heparinization; (3) rapid intra-aortic injection of dextran 40 (10 ml/kg body weight); and (4) normovelemic hemodilution with dextran 40 to a hematocrit reading of 25% to 30%. All five treated dogs awakened within 24 hours and appeared normal on the seventh day. Therapy enhanced constriction of pupils and normalization of the electroencephalogram (P less than .05). Postischemic neurological deficit is at least partially due to impaired reperfusion and can be ameliorated or prevented by blood flowing-promoting therapy.
为确定脑微循环促进疗法对缺血后脑衰竭的疗效,对11只从美索比妥钠麻醉中苏醒的犬只通过心室颤动使其经历12分钟可逆性循环骤停。复苏后对生理变量控制6小时,并对犬只观察7天。6只未接受特殊复苏后治疗的犬只未苏醒,要么在36小时内死亡,要么昏迷7天。对5只犬只采用了以下措施的组合:(1)用去甲肾上腺素将平均动脉压升至150至180毫米汞柱,持续6小时;(2)肝素化;(3)快速主动脉内注射右旋糖酐40(10毫升/千克体重);(4)用右旋糖酐40进行等容血液稀释,使血细胞比容读数达到25%至30%。所有5只接受治疗的犬只均在24小时内苏醒,且在第7天看起来正常。治疗增强了瞳孔收缩并使脑电图正常化(P小于0.05)。缺血后神经功能缺损至少部分归因于再灌注受损,可通过促进血流的疗法得到改善或预防。