MECHANISMS CAUSING SYMPATHETIC DISCHARGE DURING EXERCISE

运动期间引起交感神经放电的机制

基本信息

批准号：
2750473
负责人：
Marc Peter Kaufman
金额：
$ 23.23万
依托单位：
UNIVERSITY OF CALIFORNIA AT DAVIS
依托单位国家：
美国
项目类别：
财政年份：
1995
资助国家：
美国
起止时间：
1995-09-01 至 1999-07-31
项目状态：
已结题

项目摘要

DESCRIPTION (Applicant's abstract): A reflex arising from contracting skeletal muscle and "central command" are widely believed to be the two mechanisms that control the sympathetic nervous system during exercise. Considerable controversy exists over the contribution of each mechanism to the exercise-induced increase in sympathetic outputs to the vascular beds perfusing hindlimb skeletal muscle, hindlimb skin, and the kidney. In humans, for example, central command is thought to increase markedly sympathetic outflow to skin, but to have only a small effect on that to skeletal muscle. The reflex in contrast is thought to increase markedly the sympathetic outflow to hindlimb skeletal muscle, but to have little effect on that to the skin. There is no information in humans on the roles played by the two mechanisms in controlling renal sympathetic discharge during exercise. While recording the impulse activity of single fiber post-ganglionic fibers, we propose to compare in unanesthetized decerebrate cats, the contributions of the reflex with those of central command to sympathetic discharge during exercise. We will verify that we are recording sympathetic discharge: 1) by demonstrating that the fibers are activated by an electrical pulse applied to the thoracic or lumbar chain; 2) by demonstrating that this activation is prevented by ganglionic blockade; and 3) by demonstrating that stimulation of arterial baroreceptors inhibits baseline discharge. Central command will be elicited by either electrical or chemical stimulation of sites in the subthalamic and midbrain locomotor regions. The reflex will be elicited by low intensity electrical stimulation of peripheral nerves supplying the triceps surae muscles. The proposed experiments will test the following hypotheses. First, that the reflex, but not central command, activates sympathetic outflow to the kidney. Second, that central command, but not the reflex, activates sympathetic outflow to the skin. Third, that the reflex, but not central command, activates sympathetic outflow to non-exercising hindlimb skeletal muscle. In addition, we will be able to determine using single fiber recording techniques whether central command and the reflex impinge on the same post-ganglionic fibers. These experiments will provide, for the first time, definitive information about the roles played by central command the reflex in controlling sympathetic discharge during exercise.

描述（申请人的摘要）：收缩产生的反射骨骼肌和“中央命令”被广泛认为是两者在运动过程中控制交感神经系统的机制。每种机制的贡献存在很大的争议锻炼引起的同情输出增加了血管床为后肢骨骼肌，后肢皮肤和肾脏灌注。例如，在人类中，中央命令被认为明显增加对皮肤的同情流出，但对此只有很小的影响骨骼肌。相反，反射被认为明显增加给后肢骨骼肌的同情流出，但很少对皮肤的影响。人类没有关于这两种机制在控制肾同情方面扮演的角色运动过程中排出。在记录冲动活动的同时单光纤后纤维纤维，我们建议在未经麻醉的杂交猫，反射的贡献锻炼过程中中央指挥官要同情的那些。我们将验证我们正在记录交感神经的消除：1）证明纤维被电脉冲激活应用于胸椎或腰链； 2）证明这一点神经节封锁阻止了激活； 3）证明动脉压力受体的刺激抑制了基线排出。中央命令将通过电气或化学刺激丘脑下和中脑运动区域中的位点。反射将通过低强度的电刺激引起提供三头肌肌肉的周围神经。提议实验将检验以下假设。首先，反射，但不是中央命令，激活肾脏的同情流出。其次，该中央命令（但不是反射）激活同情流向皮肤。第三，反射，但不是中央命令，激活对非行使后肢骨骼肌的交感神经流出。此外，我们将能够使用单光纤记录来确定中央命令和反射是否侵入相同的技术后纤维纤维。这些实验将提供第一个时间，有关中央命令扮演的角色的确切信息在锻炼过程中控制交感神经消除方面的反射。