Leone J, Ochs S
J Neurobiol. 1978 May;9(3):229-45. doi: 10.1002/neu.480090305.
Axoplasmic transport of cat sciatic nerves was studied in vitro in a chamber in which maximal alpha action potentials could also be elicited. After initiation of N2 anoxia, electrical responses fell to zero at an average time of 22 min. A shorter time to zero of 11 min was seen during a second period of anoxia. A good recovery of both action potential responses and axoplasmic transport occurs after a period of anoxia lasting 1--1.5 hr. An apparent failure of recovery of axoplasmic transport was seen after 2 hr of anoxia with a good recovery of electrical responses. Axoplasmic transport tended to return toward normal when more time was allowed for recovery after anoxia. An adequate supply of approximately P was shown to be present by measurement of ATP and creatine phosphate levels. The delay in recovery of transport thus signifies a failure of utilization of approximately P by the transport mechanism. Longer periods of anoxia and recovery were limited in vitro and for this reason, ischemic anoxia was produced in vivo. Blood pressure cuffs were placed on the upper thigh of cats and maintained for times of 1--8 hr at pressures of 300-310 mm Hg. Then, recovery times up to 7 days were allowed. It was shown that axoplasmic transport could gradually recovery after an anoxia lasting up to 6-7 hr if sufficient recovery times were allowed. A possible explanation for the delay in the recovery of axoplasmic transport and the disassociation in the earlier recovery of electrical responses as against the recovery of transport was discussed.
在一个能引出最大α动作电位的小室内,对猫坐骨神经的轴浆运输进行了体外研究。在开始N₂缺氧后,电反应平均在22分钟时降至零。在第二个缺氧期,降至零的时间更短,为11分钟。持续1 - 1.5小时的缺氧期后,动作电位反应和轴浆运输都能很好地恢复。缺氧2小时后,电反应恢复良好,但轴浆运输明显未能恢复。缺氧后给予更多恢复时间时,轴浆运输倾向于恢复正常。通过测量ATP和肌酸磷酸水平表明存在充足的近似P供应。因此,运输恢复的延迟表明运输机制未能利用近似P。体外较长时间的缺氧和恢复受到限制,因此,在体内产生了缺血性缺氧。在猫的大腿上部放置血压袖带,并在300 - 310 mmHg的压力下维持1 - 8小时。然后,给予长达7天的恢复时间。结果表明,如果给予足够的恢复时间,轴浆运输在持续长达6 - 7小时的缺氧后可逐渐恢复。讨论了轴浆运输恢复延迟以及电反应早期恢复与运输恢复解离的可能原因。