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

被引:14
作者
Abe, T
Morgan, D
Sengupta, JN
Gebhart, GF
Gutterman, DD [1 ]
机构
[1] VA Med Ctr, Iowa City, IA 52242 USA
[2] Univ Iowa, Coll Med, Iowa City, IA 52242 USA
来源
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM | 1998年 / 71卷 / 01期
关键词
stunning; neural; reflex; ischemia; bradykinin; hydrogen peroxide; reperfusion;
D O I
10.1016/S0165-1838(98)00060-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 mu g), H2O2 (1.5%) or adenosine (500 mu g), 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. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:28 / 36
页数:9
相关论文
共 44 条
[21]  
KANNEL WB, 1984, NEW ENGL J MED, V311, P144
[22]  
KERR FWL, 1988, NEUROSCI RES PROG B, V16, P30
[23]   EFFECTS OF INTRA-CORONARY ADMINISTRATION OF BRADYKININ ON THE IMPULSE ACTIVITY OF AFFERENT SYMPATHETIC UNMYELINATED FIBERS WITH LEFT-VENTRICULAR ENDINGS IN THE CAT [J].
LOMBARDI, F ;
DELLABELLA, P ;
CASATI, R ;
MALLIANI, A .
CIRCULATION RESEARCH, 1981, 48 (01) :69-75
[24]   CARDIOVASCULAR SYMPATHETIC AFFERENT-FIBERS [J].
MALLIANI, A .
REVIEWS OF PHYSIOLOGY BIOCHEMISTRY AND PHARMACOLOGY, 1982, 94 :11-74
[25]   MEASUREMENTS OF CORONARY VELOCITY AND REACTIVE HYPEREMIA IN THE CORONARY CIRCULATION OF HUMANS [J].
MARCUS, M ;
WRIGHT, C ;
DOTY, D ;
EASTHAM, C ;
LAUGHLIN, D ;
KRUMM, P ;
FASTENOW, C ;
BRODY, M .
CIRCULATION RESEARCH, 1981, 49 (04) :877-891
[26]  
MASERI A, 1987, ACTA CARDIOL, V42, P153
[27]   A CRITICAL-REVIEW OF THE AFFERENT PATHWAYS AND THE POTENTIAL CHEMICAL MEDIATORS INVOLVED IN CARDIAC PAIN [J].
MELLER, ST ;
GEBHART, GF .
NEUROSCIENCE, 1992, 48 (03) :501-524
[28]   Oxygen-derived free radicals contribute to neural stunning in the canine heart [J].
Miura, H ;
Morgan, DA ;
Gutterman, DD .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 273 (03) :H1569-H1575
[29]   PRESYNAPTIC MODULATION OF EFFERENT SYMPATHETIC AND VAGAL NEUROTRANSMISSION IN THE CANINE HEART BY HYPOXIA, HIGH K+, LOW PH, AND ADENOSINE - POSSIBLE RELEVANCE TO ISCHEMIA-INDUCED DENERVATION [J].
MIYAZAKI, T ;
ZIPES, DP .
CIRCULATION RESEARCH, 1990, 66 (02) :289-301
[30]   ADRENERGIC VASOCONSTRICTION LESSENS TRANSMURAL STEAL DURING CORONARY HYPOPERFUSION [J].
NATHAN, HJ ;
FEIGL, EO .
AMERICAN JOURNAL OF PHYSIOLOGY, 1986, 250 (04) :H645-H653