EFFECT OF NOREPINEPHRINE ON CONTRACTILITY OF ISOLATED MESENTERIC LYMPHATICS
EFFECT OF NOREPINEPHRINE ON CONTRACTILITY OF ISOLATED MESENTERIC LYMPHATICS
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DOI：
10.1152/ajpheart.1983.244.4.h479
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发表时间：
1983-01-01
影响因子：
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通讯作者：
ROONEY, BM
中科院分区：
文献类型：
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作者：
ALLEN, JM;MCHALE, NG;ROONEY, BM
去甲肾上腺素增加了牛淋巴管的自发收缩频率，但矛盾的是，却降低了收缩力量。在这项研究中，收缩是由电刺激引起的，作为场刺激或跨越蔗糖间隙。去甲肾上腺素的浓度不能有效地减少诱发的收缩，而去甲肾上腺素此前已被证明会显著降低自发活动的血管的收缩能力。然而，在较高浓度时，经常观察到去甲肾上腺素效应中的β抑制成分。自发活动血管的电活动和机械活动的同时记录表明，每一次自发收缩都是由单一动作电位启动的。去甲肾上腺素显著干扰电活动，导致动作电位频率增加，动作电位幅度降低，全动作电位发育经常失败。显然，去甲肾上腺素通过破坏自发起搏而不是通过对血管收缩的任何直接作用来抑制自发收缩的力量。
Norepinephrine increases the spontaneous contraction frequency of isolated bovine lymphatic vessels, but paradoxically, reduces contraction force. In this investigation contractions were elicited by electrical stimulation, applied as field stimulation or across a sucrose gap. Evoked contractions were not reduced in force by concentrations of norepinephrine that have previously been shown to dramatically reduce contractility in spontaneously active vessels. However, at higher concentrations a .beta.-inhibitory component of the norepinephrine effect was often observed. Simultaneous recordings of electrical and mechanical activity from spontaneously active vessels showed that each spontaneous contraction was initiated by a single action potential. Norepinephrine significantly disrupted electrical activity causing increased action potential frequency, reduction in action potential amplitude and frequent failure of full action potential development. Apparently, norepinephrine depresses the force of spontaneous contractions by disruption of spontaneous pacemaking rather than by any direct effect on vessel contractility.