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The effect of age on energy metabolism and resistance to ischaemic conduction failure in rat peripheral nerve.

机译:年龄对大鼠周围神经能量代谢和对缺血性传导衰竭抵抗力的影响。

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摘要

Caudal nerve conduction velocity and amplitude of nerve action potential increased progressively with age to 8 months after which time no further increases were demonstrated. Rat peripheral nerve was progressively more resistant to ischaemic-anoxic conduction failure with increasing age. This resistance to ischaemic conduction failure was paralleled by a progressive age-related decline in endoneurial O2 consumption. Endoneurial adenosine triphosphate and creatine phosphate values were also progressively reduced with age. 15 min of anoxia resulted in progressively smaller reductions in these nucleotide phosphates with increasing age to 8 months after which time little further change occurred. Nerve lactate response to anoxia was higher in young rats (1 and 2 months) than in older animals (8 and 21 months). High energy phosphate expenditure progressively declined with age to 8 months, then stabilized. These findings indicate that the major mechanism of resistance to ischaemic conduction failure is a progressive decline in energy requirements.
机译:尾神经传导速度和神经动作电位的幅度随着年龄的增长而逐渐增加,至8个月后没有进一步增加。随着年龄的增长,大鼠周围神经对缺血-缺氧传导衰竭的抵抗力逐渐增强。这种对缺血性传导衰竭的抵抗力与年龄相关的神经内膜O2消耗量的逐步下降相平行。随着年龄的增长,神经内膜三磷酸腺苷和磷酸肌酸的值也逐渐降低。 15分钟的缺氧会导致这些核苷酸磷酸酯的减少程度逐渐减小,随着年龄的增长而增加,直至8个月,此后几乎没有进一步的变化。幼年大鼠(1和2个月)中神经乳酸对缺氧的反应高于年长动物(8和21个月)。高能磷酸盐支出随着年龄的增长逐渐下降至8个月,然后稳定下来。这些发现表明,抵抗局部缺血性传导衰竭的主要机制是能量需求的逐步下降。

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