Amelioration of brain damage after 12 minutes' cardiac arrest in dogs.
Amelioration of brain damage after 12 minutes' cardiac arrest in dogs.
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改善狗心脏骤停 12 分钟后的脑损伤。
DOI：
10.1001/archneur.1976.00500020019004
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发表时间：
1976
影响因子：
--
通讯作者：
E. Nemoto
中科院分区：
文献类型：
--
作者：
P. Safar;W. Stezoski;E. Nemoto
为探讨脑微循环促进疗法对缺血后脑功能衰竭的疗效，对11只从美索比妥钠麻醉中苏醒的狗进行了可逆性停循环12分钟的室颤试验。复苏后6小时内控制生理变量，观察犬7天。6只没有接受特殊复苏后治疗的狗没有醒来，要么在36小时内死亡，要么昏迷7天。在5只犬中，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高至150至180 mm Hg，持续6小时;（2）肝素化;（3）快速主动脉内注射右旋糖酐40（10 ml/kg体重）;和（4）用右旋糖酐40进行正常血流量血液稀释，使红细胞压积阅读为25%至30%。所有5只接受治疗的犬均在24小时内苏醒，并在第7天表现正常。治疗增强了瞳孔收缩和脑电图正常化（P <0.05）。缺血后神经功能缺损至少部分是由于再灌注受损，可以通过促进血流治疗来改善或预防。
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.