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猫短暂心肌缺血后缺血诱导的心脏交感传入神经激活的减弱

Attenuation of ischemia-induced activation of cardiac sympathetic afferents following brief myocardial ischemia in cats.

作者信息

Abe T, Morgan D, Sengupta J N, Gebhart G F, Gutterman D D

机构信息

VA Med. Ctr. and University of Iowa College of Medicine, Iowa City 52242, USA.

出版信息

J Auton Nerv Syst. 1998 Jun 30;71(1):28-36. doi: 10.1016/s0165-1838(98)00060-5.

Abstract

OBJECTIVE

We have previously shown that brief myocardial ischemia impairs neural conduction in cardiac sympathetic efferent fibers. However, attenuation of the activity of afferent sympathetic nerves, which may contribute to impaired ischemic nociception and reflex hemodynamic responses, is not well understood. Therefore, we studied the electrophysiological effects of brief myocardial ischemia on the mechano-, chemo- and ischemia-sensitive properties of cardiac sympathetic afferent fibers.

METHODS

Single unit activity of sympathetic afferent A delta and C fibers innervating the left ventricle (LV) was recorded from the thoracic chain or rami communicantes in 16 anesthetized cats. We tested the response of impulse activity to (1) mechanical LV probing, (2) epicardial application of bradykinin (10 microg), H2O2 (1.5%) or adenosine (500 microg), and (3) 1 min of coronary occlusion. Repeat tests were performed in 11 of 16 fibers after 15 min of coronary occlusion and 15 min of reperfusion. Control responses were measured in five fibers before and after a 30-min interval without ischemia.

RESULTS

Afferent fibers responded with increased activity to LV probing (16/16 fibers), bradykinin (13/16 fibers), H2O2 (7/11 fibers), adenosine (1/11 fibers), and to a 60 s period of coronary occlusion (11/16 fibers). The unit impulse activity to 1 min of coronary occlusion was markedly attenuated after 15 min of myocardial ischemia and 15 min of reperfusion (P < 0.05). This attenuation was associated with reduced sensitivity to mechanical and chemical stimuli, while in separate time-control studies (n = 5) no attenuation was observed in absence of ischemia.

CONCLUSION

A brief period of myocardial ischemia is capable of attenuating mechano-, chemo- and ischemia-sensitive activity of cardiac afferent sympathetic nerves. This may have important implications for the mechanism of silent myocardial ischemia.

摘要

目的

我们之前已经表明,短暂的心肌缺血会损害心脏交感传出纤维的神经传导。然而,传入交感神经活动的减弱,这可能导致缺血性伤害感受和反射性血流动力学反应受损,目前尚未完全清楚。因此,我们研究了短暂心肌缺血对心脏交感传入纤维的机械、化学和缺血敏感性特性的电生理影响。

方法

在16只麻醉猫的胸段交感神经链或交通支记录支配左心室(LV)的交感传入Aδ和C纤维的单单位活动。我们测试了冲动活动对以下刺激的反应:(1)左心室机械探查,(2)在心外膜应用缓激肽(10微克)、过氧化氢(1.5%)或腺苷(500微克),以及(3)冠状动脉闭塞1分钟。在16根纤维中的11根纤维在冠状动脉闭塞15分钟和再灌注15分钟后进行重复测试。在5根纤维上,在无缺血的30分钟间隔前后测量对照反应。

结果

传入纤维对左心室探查(16/16根纤维)、缓激肽(13/16根纤维)、过氧化氢(7/11根纤维)、腺苷(1/11根纤维)以及冠状动脉闭塞60秒(11/16根纤维)的反应是活动增加。在心肌缺血15分钟和再灌注15分钟后,冠状动脉闭塞1分钟的单位冲动活动明显减弱(P<0.05)。这种减弱与对机械和化学刺激的敏感性降低有关,而在单独的时间对照研究(n = 5)中,在无缺血的情况下未观察到减弱。

结论

短暂的心肌缺血能够减弱心脏传入交感神经的机械、化学和缺血敏感性活动。这可能对无症状心肌缺血的机制具有重要意义。

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