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缺氧对猫Ⅲ类和Ⅳ类肌肉传入神经放电的影响。

Effects of hypoxia on the discharge of group III and IV muscle afferents in cats.

作者信息

Hill J M, Pickar J G, Parrish M D, Kaufman M P

机构信息

Division of Cardiovascular Medicine, University of California, Davis 95616.

出版信息

J Appl Physiol (1985). 1992 Dec;73(6):2524-9. doi: 10.1152/jappl.1992.73.6.2524.

Abstract

The reflex pressor response evoked by static muscular contraction is widely believed to be caused by the stimulation of group III and IV afferents. Although the specific nature of the contraction-induced stimulus to these thin-fiber afferents is unknown, they are thought to be stimulated in part by a condition arising from a mismatch between blood supply and demand in the exercising muscle. Hypoxia, a condition found in skeletal muscle during such a mismatch, may stimulate these afferents. We have therefore tested the hypothesis that perfusion of the triceps surae muscles with hypoxic blood stimulates group III and IV afferents in barbiturate-anesthetized cats. We found that 3-3.5 min of hypoxia with the triceps surae muscles at rest significantly (P < 0.05) increased the average discharge rate of contraction-sensitive group IV afferents but had no effect on the average discharge rate of contraction-sensitive group III afferents. Hypoxia had only trivial effects on the discharge of contraction-insensitive group III and IV afferents. Hypoxia stimulated 4 of 11 contraction-sensitive group IV afferents and 2 of 13 contraction-sensitive group III afferents. The responses of the afferents stimulated by hypoxia were small in magnitude. Hypoxia with the muscles at rest appeared to have no effect on either hydrogen or lactate ion concentrations in the femoral venous blood. In addition, hypoxia increased the responses to contraction in only 3 of 22 group III and 4 of 21 group IV afferents tested. We conclude that muscle tissue hypoxia is a minor stimulus to afferents that sense a mismatch between blood supply and demand during static contraction.

摘要

人们普遍认为,静态肌肉收缩引起的反射性升压反应是由Ⅲ类和Ⅳ类传入神经的刺激所导致的。尽管尚不清楚收缩对这些细纤维传入神经所诱发刺激的具体性质,但一般认为部分原因是运动肌肉中血液供应与需求不匹配所产生的一种状况。低氧血症是在这种不匹配期间骨骼肌中出现的一种状况,可能会刺激这些传入神经。因此,我们检验了这样一个假设:用低氧血液灌注腓肠肌会刺激巴比妥麻醉猫的Ⅲ类和Ⅳ类传入神经。我们发现,在腓肠肌处于静息状态下进行3 - 3.5分钟的低氧处理,显著(P < 0.05)增加了对收缩敏感的Ⅳ类传入神经的平均放电率,但对收缩敏感的Ⅲ类传入神经的平均放电率没有影响。低氧对不敏感于收缩的Ⅲ类和Ⅳ类传入神经的放电只有轻微影响。低氧刺激了11根对收缩敏感的Ⅳ类传入神经中的4根和13根对收缩敏感的Ⅲ类传入神经中的2根。低氧刺激引起的传入神经反应幅度较小。肌肉处于静息状态下的低氧似乎对股静脉血中的氢离子或乳酸离子浓度均无影响。此外,在接受测试的22根Ⅲ类传入神经中,低氧仅增强了其中3根对收缩的反应,在21根Ⅳ类传入神经中仅增强了4根对收缩的反应。我们得出结论,在静态收缩过程中,肌肉组织低氧是对感知血液供应与需求不匹配的传入神经的一种次要刺激。

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