LOCAL CEREBRAL BLOOD-FLOW DURING HIBERNATION, A MODEL OF NATURAL TOLERANCE TO CEREBRAL-ISCHEMIA
LOCAL CEREBRAL BLOOD-FLOW DURING HIBERNATION, A MODEL OF NATURAL TOLERANCE TO CEREBRAL-ISCHEMIA
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DOI：
10.1038/jcbfm.1994.26
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发表时间：
1994-03-01
影响因子：
6.3
通讯作者：
HALLENBECK, JM
中科院分区：
文献类型：
--
作者：
FRERICHS, KU;KENNEDY, C;HALLENBECK, JM
脑缺血时细胞内稳态的破坏和进行性神经元的破坏似乎是由错综复杂的相互关联的原因组成的复杂网络所介导的。我们研究了自然界中正常存在的一种生理状态，在这种状态下，哺乳动物似乎耐受缺血的通常有害影响，并减少氧气的可获得性，并抵抗自毁过程的激活，即哺乳动物冬眠。地鼠(Spermophilus Tridecemlineatus)被长期植入动静脉导管和遥测装置，用于脑电、心电和体温监测。这些动物被放置在环境温度为5摄氏度的环境中，进入冬眠的特征是心率下降，随后体温逐渐下降，并进行等电脑电检查。不冬眠的冷适应活动动物作为对照。采用放射自显影[C-14]碘安替比林法测定脑血流量(CBF)。对照组平均(+/-SD)脑血流量为62+/-16ml/100g/分钟(n=4)，而冬眠动物(P<；0.001)则降至缺血水平7+/-4ml/100g/分钟(n=4)。在从冬眠中唤醒的类似冬眠动物中，没有发现神经病理变化。冬眠似乎受到了积极的调节，可能与荷尔蒙因素有关。识别和表征这些因素以及冬眠物种用来增加缺血耐受性和钝化缺血破坏效应的机制，可能使我们能够防止或最大限度地减少其他物种在脑缺血过程中和脑缺血后动态平衡控制的丧失。
The breakdown of cellular homeostasis and progressive neuronal destruction in cerebral ischemia appears to be mediated by a complex network of causes that are intricately interrelated. We have investigated a physiological state existing normally in nature in which mammals appear to tolerate the ordinarily detrimental effects of ischemia with reduced oxygen availability and to resist activation of self-destructive processes, i.e., mammalian hibernation. Ground squirrels (Spermophilus tridecemlineatus) were chronically implanted with arterial and ve nous catheters and telemetry devices for electroencephalography, electrocardiography, and monitoring of body temperature. The animals were placed in an environmental chamber at an ambient temperature of 5 degrees C. Entrance into hibernation was characterized by a drop in heart rate followed by a gradual decline in body temperature and an isoelectric electroencephalogram. Cold-adapted active animals that were not hibernating served as controls. Cerebral blood flow (CBF) was measured in both groups with the autoradiographic [C-14]iodoantipyrine method. Mean (+/- SD) mass-weighted CBF in the brain as a whole was 62 +/- 16 ml/100 g/min (n = 4) in the control group but was reduced to ischemic levels, 7 +/- 4 ml/100 g/min (n = 4), in the hibernating animals (p < 0.001). No neuropathological changes were found in similarly hibernating animals aroused from hibernation. Hibernation appears to be actively regulated, and hormonal factors may be involved. The identification and characterization of such factors and of the mechanisms used by hibernating species to increase ischemic tolerance and to blunt the destructive effects of ischemia may enable us to prevent or minimize the loss of homeostatic control during and after cerebral ischemia in other species.