Towfighi J, Vannucci R C
Department of Pathology (Neuropathology), Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey 17033-0850, USA.
Acta Neuropathol. 1997 May;93(5):485-93. doi: 10.1007/s004010050643.
Neuropathologic findings are described, for the first time, in a neonatal dog model of circulatory arrest in normothermic conditions, and the findings are compared to those reported in neonatal dogs with hypothermic circulatory arrest. Total circulatory arrest was produced in 3- to 6-day-old anesthetized, paralyzed and ventilated, normothermic dogs either by asphyxiation or cardioplegia. Duration of circulatory arrest was 8-20 min and 10-40 min in asphyxiated and cardioplegic animals, respectively. The animals were resuscitated and maintained under controlled systemic physiologic conditions until neuropathologic examination after 8 or 24 h of recovery. The results suggest that the minimal durations of circulatory arrest for brain damage to occur following asphyxia or cardioplegia are 10 and 15 min, respectively. Ischemic lesions in both groups consisted of neuronal necrosis and involved mainly the brain stem structures, particularly the reticular nuclei and the spinal cord gray matter. The medulla was more severely involved than midbrain and pons. There was a direct correlation between the length of circulatory arrest and the severity of damage in the medulla (P = 0.001) and overall brain stem damage (P = 0.004) in animals with cardioplegia, but not in animals with asphyxia. These findings are compared to the neuropathologic changes previously described in newborn dogs subjected to hypothermic circulatory arrest, in which ischemic lesions are focused on the cerebral cortex and basal ganglia. It is concluded that hypothermia in this model not only prolongs the period of circulatory arrest that is required to produce brain damage, but also shifts the pattern of regional ischemic vulnerability from caudal to more rostral structures.
首次在正常体温条件下循环骤停的新生犬模型中描述了神经病理学发现，并将这些发现与低温循环骤停的新生犬报告的发现进行了比较。通过窒息或心脏停搏，在3至6日龄麻醉、麻痹并通气的正常体温犬中产生完全循环骤停。窒息和心脏停搏动物的循环骤停持续时间分别为8至20分钟和10至40分钟。动物复苏后，在受控的全身生理条件下维持，直至恢复8或24小时后进行神经病理学检查。结果表明，窒息或心脏停搏后发生脑损伤的循环骤停最短持续时间分别为10分钟和15分钟。两组的缺血性病变均包括神经元坏死，主要累及脑干结构，特别是网状核和脊髓灰质。延髓比中脑和脑桥受累更严重。心脏停搏动物的延髓损伤严重程度（P = 0.001）和整体脑干损伤（P = 0.004）与循环骤停时间长度之间存在直接相关性，但窒息动物不存在这种相关性。将这些发现与先前描述的经历低温循环骤停的新生犬的神经病理学变化进行比较，在低温循环骤停中，缺血性病变集中在大脑皮层和基底神经节。得出的结论是，该模型中的低温不仅延长了产生脑损伤所需的循环骤停时间，而且将局部缺血易损性模式从尾部结构转移到了更靠前的结构。
