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大鼠颈动脉体的低氧适应

Hypoxic adaptation of the rat carotid body.

作者信息

Kusakabe T, Matsuda H, Hayashida Y

机构信息

Laboratory for Anatomy and Physiology, Department of Sport and Medical Science, Kokushikan University, 7-3-1 Nagayama, Tama, Tokyo 206-8515, Japan.

出版信息

Histol Histopathol. 2005 Jul;20(3):987-97. doi: 10.14670/HH-20.987.

Abstract

Three types of hypoxia with different levels of carbon dioxide (hypocapnic, isocapnic, and hypercapnic hypoxia) have been called systemic hypoxia. The systemic hypoxic carotid bodies were enlarged several fold, but the degree of enlargement was different for each. The mean short and long axes of hypocapnic and isocapnic hypoxic carotid bodies were 1.6 (short axis) and 1.8-1.9 (long axis) times larger than normoxic control carotid bodies, respectively. Those of hypercapnic hypoxic carotid bodies were 1.2 (short axis) and 1.5 (long axis) times larger than controls, respectively. The rate of enlargement in hypercapnic hypoxic carotid bodies was lower than in hypocapnic and isocapnic hypoxic carotid bodies. The rate of vascular enlargement in hypercapnic hypoxic carotid bodies was also smaller than in hypocapnic and isocapnic hypoxic carotid bodies. Thus, the enlargement of hypoxic carotid bodies is mainly due to vascular dilation. Different levels of arterial CO2 tension change the peptidergic innervation during chronically hypoxic exposure. The characteristic vascular arrangement was under the control of altered peptidergic innervation. During the course of hypoxic adaptation, the enlargement of the carotid bodies with vascular expansion began soon after the start of hypoxic exposure. During the course of recovery, the shrinking of the carotid bodies with vascular contraction also started at a relatively early period after the termination of chronic hypoxia. These processes during the course of hypoxic adaptation and during the course of recovery were under the control of peptidergic innervation. These findings may provide a standard for further studies of hypoxic carotid bodies.

摘要

三种不同二氧化碳水平的低氧血症(低碳酸血症性、等碳酸血症性和高碳酸血症性低氧血症)被称为全身性低氧血症。全身性低氧的颈动脉体增大了几倍,但每种类型的增大程度不同。低碳酸血症性和等碳酸血症性低氧颈动脉体的平均短轴和长轴分别比常氧对照颈动脉体大1.6倍(短轴)和1.8 - 1.9倍(长轴)。高碳酸血症性低氧颈动脉体的短轴和长轴分别比对照大1.2倍(短轴)和1.5倍(长轴)。高碳酸血症性低氧颈动脉体的增大速率低于低碳酸血症性和等碳酸血症性低氧颈动脉体。高碳酸血症性低氧颈动脉体的血管增大速率也小于低碳酸血症性和等碳酸血症性低氧颈动脉体。因此,低氧颈动脉体的增大主要是由于血管扩张。不同水平的动脉二氧化碳张力在慢性低氧暴露期间会改变肽能神经支配。特征性的血管排列受肽能神经支配改变的控制。在低氧适应过程中,随着血管扩张,颈动脉体的增大在低氧暴露开始后不久就开始了。在恢复过程中,随着血管收缩,颈动脉体的缩小也在慢性低氧终止后的相对早期开始。低氧适应过程和恢复过程中的这些变化受肽能神经支配的控制。这些发现可能为进一步研究低氧颈动脉体提供一个标准。

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