ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009
Cardiac damage after lesions of the nucleus tractus solitarii.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Parasubthalamic Glutamatergic Neurons Coordinate Cardiovascular Homeostasis and Locomotion in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Tangled History of Brain-Heart Pathways in Acute Brain Injury.Neurocritical care · 2023Article
- Article
- Chemosensitive Phox2b-expressing neurons are crucial for hypercapnic ventilatory response in the nucleus tractus solitarius.The Journal of physiology · 2017Article
- Reduced responses to glutamate receptor agonists follow loss of astrocytes and astroglial glutamate markers in the nucleus tractus solitarii.Physiological reports · 2017Article
- Astrocytes in the rat nucleus tractus solitarii are critical for cardiovascular reflex control.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Sudden death following selective neuronal lesions in the rat nucleus tractus solitarii.Autonomic neuroscience : basic & clinical · 2013Review
- Sudden death and myocardial lesions after damage to catecholamine neurons of the nucleus tractus solitarii in rat.Cellular and molecular neurobiology · 2012Article
- Views of translational research from a somewhat translational scientist.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2012Review
- Decreased expression of neuronal nitric oxide synthase in the nucleus tractus solitarii inhibits sympathetically mediated baroreflex responses in rat.The Journal of physiology · 2012Article
- Collateral damage and compensatory changes after injection of a toxin targeting neurons with the neurokinin-1 receptor in the nucleus tractus solitarii of rat.Journal of chemical neuroanatomy · 2012Article
- Targeted ablation of mesenteric projecting sympathetic neurons reduces the hemodynamic response to pain in conscious, spinal cord-transected rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Targeted ablation of cardiac sympathetic neurons reduces the susceptibility to ischemia-induced sustained ventricular tachycardia in conscious rats.American journal of physiology. Heart and circulatory physiology · 2010Article
- Targeted ablation of cardiac sympathetic neurons reduces resting, reflex and exercise-induced sympathetic activation in conscious rats.American journal of physiology. Heart and circulatory physiology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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 approximately 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.
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