Inhibitory mechanism of slowly adapting pulmonary stretch receptors after release from hyperinflation in anesthetized rabbits

被引:11
|
作者
Matsumoto, S [1 ]
Ikeda, M [1 ]
Nishikawa, T [1 ]
Tanimoto, T [1 ]
Yoshida, S [1 ]
Saiki, C [1 ]
机构
[1] Nippon Dent Univ, Sch Dent Tokyo, Dept Physiol, Chiyoda Ku, Tokyo 1028159, Japan
关键词
slowly adapting pulmonary stretch receptor; slow afterhyperpolarization; hyperinflation; potassium channel blocker; sodium pump;
D O I
10.1016/S0024-3205(00)00738-4
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
In anesthetized, artificially ventilated rabbits with vagus nerve section, release from 10 consecutive hyper;inflations (inflation volume = 3 tidal volume) caused an inhibition of the slowly adapting pulmonary stretch receptor (SAR) activity for 16-22 sec. Intravenous administration of tetraethylammonium (TEA, 10 and 20 mg/kg), a K+ channel blocker, did not significantly alter either basal SAR discharge or tracheal pressure (PT) Although TEA treatment at 10.0 mg/kg had no significant effect on the magnitude and duration of inhibited SAR activity seen after release from hyperinflation, the increasing dose of this K+ channel blocker up to 20 mg/kg inhibited these effects of the receptor activity but this inhibition was small. The Na+-K+ ATPase inhibitor ouabain (5 and 10 mu g/kg) that had no significant effect on SAR activity and PT ill the control abolished or attenuated the inhibitory action of SARs in a dose-dependent manner. Furthermore, the changes in dynamic lung compliance (Cdyn) and P-T in response to post-hyperinflation were not significantly influenced by pretreatment with either TEA or ouabain. These results suggest that the inhibitory action of receptors seen during post-hyperinflation corresponded with the induction of slow afterhyperpolarization (sAHP), and that the mechanism of generating the sAHP of SARs is mainly mediated by the activation of Na+-K+ pump activity. (C) 2000 Elsevier Science Inc. All rights reserved.
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页码:1423 / 1433
页数:11
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