Cardiac damage after lesions of the nucleus tractus solitarii

Ameya Nayate; Steven A Moore; Robert Weiss; Otar M Taktakishvili; Li-Hsien Lin; William T Talman

doi:10.1152/ajpregu.00080.2008

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Cardiac damage after lesions of the nucleus tractus solitarii

Journal article

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Peer reviewed

Cardiac damage after lesions of the nucleus tractus solitarii

Ameya Nayate, Steven A Moore, Robert Weiss, Otar M Taktakishvili, Li-Hsien Lin and William T Talman

American journal of physiology. Regulatory, integrative and comparative physiology, Vol.296(2), pp.R272-R279

02/2009

DOI: 10.1152/ajpregu.00080.2008

PMCID: PMC2643979

PMID: 19020288

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Abstract

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.

sudden death

Hemodynamics and Cardiorenal Integration

baroreflex

cardiac arrhythmia

sympathetic nervous system

heart injuries

Details

Title: Subtitle: Cardiac damage after lesions of the nucleus tractus solitarii
Creators: Ameya Nayate - Departments of
Steven A Moore - Departments of
Robert Weiss - Departments of
Otar M Taktakishvili - Departments of
Li-Hsien Lin - Departments of
William T Talman - Departments of
Resource Type: Journal article
Publication Details: American journal of physiology. Regulatory, integrative and comparative physiology, Vol.296(2), pp.R272-R279
DOI: 10.1152/ajpregu.00080.2008
PMID: 19020288
PMCID: PMC2643979
NLM abbreviation: Am J Physiol Regul Integr Comp Physiol
ISSN: 0363-6119
eISSN: 1522-1490
Publisher: American Physiological Society
Language: English
Date published: 02/2009
Academic Unit: Neurology; Pathology; Cardiovascular Medicine; Internal Medicine
Record Identifier: 9984047799902771

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