HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 296/2/R272    most recent 00080.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nayate, A. Articles by Talman, W. T. Search for Related Content PubMed PubMed Citation Articles by Nayate, A. Articles by Talman, W. T.

HEMODYNAMICS AND CARDIORENAL INTEGRATION

Cardiac damage after lesions of the nucleus tractus solitarii

Departments of ¹Neurology, ²Pathology, and ³Internal Medicine, University of Iowa and Veterans Affairs Health Care System, Iowa City, Iowa

Submitted 4 February 2008 ; accepted in final form 12 November 2008

Humans with central lesions that augment sympathetic nerve activity are predisposed to cardiac arrhythmias, myocardial lesions, and sudden death. Previously, we showed that selectively killing neurons with neurokinin-1 receptors in the nucleus tractus solitarii (NTS) of rats attenuated the baroreflex and, in some animals, led to sudden unexplained death within 2 wk. Interruption of arterial baroreflexes is known to increase sympathetic activity. Here we tested the hypothesis that lesions in the NTS lead to fatal cardiac arrhythmias and myocardial lesions. We studied electrocardiograms, echocardiograms, blood pressure, and heart rate in 14 adult male rats after bilateral microinjection into the NTS of stabilized substance P conjugated to the toxin saporin and compared the variables in five sham control rats and in five animals with toxin injected outside the NTS. Only injection of toxin into the NTS led to increased lability of arterial blood pressure, a sign of baroreflex interruption. Two animals treated with toxin died suddenly. All animals engaged in normal activity until, in two, rapid development of asystole and death over 6–8 min. Cardiac function when examined by echocardiography was normal, but pathologic examination of the heart revealed diffuse microscopic areas of acute coagulation necrosis in the myocardium in five animals, focal subacute necrosis in two animals, and both changes in one animal. This study supports the hypothesis that NTS lesions interrupting the baroreflex may induce cardiac arrhythmias and myocardial changes similar to those seen in humans with central lesions and may lead to sudden cardiac death.

baroreflex; cardiac arrhythmia; heart injuries; sudden death; sympathetic nervous system

This article has been cited by other articles:

				H. L. Lujan, G. Palani, Y. Chen, J. D. Peduzzi, and S. E. DiCarlo Targeted ablation of cardiac sympathetic neurons reduces resting, reflex and exercise-induced sympathetic activation in conscious rats Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1305 - H1311. [Abstract] [Full Text] [PDF]