Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest
Sudden cardiac arrest is a leading cause of death in the United States. The neurophysiological mechanism underlying sudden death is not well understood. Previously we have shown that the brain is highly stimulated in dying animals and that asphyxia-induced death could be delayed by blocking the inta...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2018-02-01
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| Series: | Frontiers in Physiology |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/article/10.3389/fphys.2018.00099/full |
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Article |
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DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Fangyun Tian Tiecheng Liu Gang Xu Duan Li Talha Ghazi Trevor Shick Azeem Sajjad Michael M. Wang Michael M. Wang Michael M. Wang Michael M. Wang Michael M. Wang Peter Farrehi Peter Farrehi Jimo Borjigin Jimo Borjigin Jimo Borjigin Jimo Borjigin Jimo Borjigin |
| spellingShingle |
Fangyun Tian Tiecheng Liu Gang Xu Duan Li Talha Ghazi Trevor Shick Azeem Sajjad Michael M. Wang Michael M. Wang Michael M. Wang Michael M. Wang Michael M. Wang Peter Farrehi Peter Farrehi Jimo Borjigin Jimo Borjigin Jimo Borjigin Jimo Borjigin Jimo Borjigin Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest Frontiers in Physiology atenolol phentolamine autonomic nervous system coherence directional connectivity asphyxic cardiac arrest |
| author_facet |
Fangyun Tian Tiecheng Liu Gang Xu Duan Li Talha Ghazi Trevor Shick Azeem Sajjad Michael M. Wang Michael M. Wang Michael M. Wang Michael M. Wang Michael M. Wang Peter Farrehi Peter Farrehi Jimo Borjigin Jimo Borjigin Jimo Borjigin Jimo Borjigin Jimo Borjigin |
| author_sort |
Fangyun Tian |
| title |
Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest |
| title_short |
Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest |
| title_full |
Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest |
| title_fullStr |
Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest |
| title_full_unstemmed |
Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest |
| title_sort |
adrenergic blockade bi-directionally and asymmetrically alters functional brain-heart communication and prolongs electrical activities of the brain and heart during asphyxic cardiac arrest |
| publisher |
Frontiers Media S.A. |
| series |
Frontiers in Physiology |
| issn |
1664-042X |
| publishDate |
2018-02-01 |
| description |
Sudden cardiac arrest is a leading cause of death in the United States. The neurophysiological mechanism underlying sudden death is not well understood. Previously we have shown that the brain is highly stimulated in dying animals and that asphyxia-induced death could be delayed by blocking the intact brain-heart neuronal connection. These studies suggest that the autonomic nervous system plays an important role in mediating sudden cardiac arrest. In this study, we tested the effectiveness of phentolamine and atenolol, individually or combined, in prolonging functionality of the vital organs in CO2-mediated asphyxic cardiac arrest model. Rats received either saline, phentolamine, atenolol, or phentolamine plus atenolol, 30 min before the onset of asphyxia. Electrocardiogram (ECG) and electroencephalogram (EEG) signals were simultaneously collected from each rat during the entire process and investigated for cardiac and brain functions using a battery of analytic tools. We found that adrenergic blockade significantly suppressed the initial decline of cardiac output, prolonged electrical activities of both brain and heart, asymmetrically altered functional connectivity within the brain, and altered, bi-directionally and asymmetrically, functional, and effective connectivity between the brain and heart. The protective effects of adrenergic blockers paralleled the suppression of brain and heart connectivity, especially in the right hemisphere associated with central regulation of sympathetic function. Collectively, our results demonstrate that blockade of brain-heart connection via alpha- and beta-adrenergic blockers significantly prolonged the detectable activities of both the heart and the brain in asphyxic rat. The beneficial effects of combined alpha and beta blockers may help extend the survival of cardiac arrest patients. |
| topic |
atenolol phentolamine autonomic nervous system coherence directional connectivity asphyxic cardiac arrest |
| url |
http://journal.frontiersin.org/article/10.3389/fphys.2018.00099/full |
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doaj-d2bd29e19ecf4ebb9e517f05909edf812020-11-24T21:51:55ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2018-02-01910.3389/fphys.2018.00099255514Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac ArrestFangyun Tian0Tiecheng Liu1Gang Xu2Duan Li3Talha Ghazi4Trevor Shick5Azeem Sajjad6Michael M. Wang7Michael M. Wang8Michael M. Wang9Michael M. Wang10Michael M. Wang11Peter Farrehi12Peter Farrehi13Jimo Borjigin14Jimo Borjigin15Jimo Borjigin16Jimo Borjigin17Jimo Borjigin18Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Neurology, University of Michigan, Ann Arbor, MI, United StatesNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, United StatesCardiovascular Center, University of Michigan, Ann Arbor, MI, United StatesVeterans Administration Ann Arbor Healthcare System, Ann Arbor, MI, United StatesCardiovascular Center, University of Michigan, Ann Arbor, MI, United StatesDepartment of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesDepartment of Neurology, University of Michigan, Ann Arbor, MI, United StatesNeuroscience Graduate Program, University of Michigan, Ann Arbor, MI, United StatesCardiovascular Center, University of Michigan, Ann Arbor, MI, United StatesMichigan Center for Integrative Research in Critical Care, University of Michigan, Ann Arbor, MI, United StatesSudden cardiac arrest is a leading cause of death in the United States. The neurophysiological mechanism underlying sudden death is not well understood. Previously we have shown that the brain is highly stimulated in dying animals and that asphyxia-induced death could be delayed by blocking the intact brain-heart neuronal connection. These studies suggest that the autonomic nervous system plays an important role in mediating sudden cardiac arrest. In this study, we tested the effectiveness of phentolamine and atenolol, individually or combined, in prolonging functionality of the vital organs in CO2-mediated asphyxic cardiac arrest model. Rats received either saline, phentolamine, atenolol, or phentolamine plus atenolol, 30 min before the onset of asphyxia. Electrocardiogram (ECG) and electroencephalogram (EEG) signals were simultaneously collected from each rat during the entire process and investigated for cardiac and brain functions using a battery of analytic tools. We found that adrenergic blockade significantly suppressed the initial decline of cardiac output, prolonged electrical activities of both brain and heart, asymmetrically altered functional connectivity within the brain, and altered, bi-directionally and asymmetrically, functional, and effective connectivity between the brain and heart. The protective effects of adrenergic blockers paralleled the suppression of brain and heart connectivity, especially in the right hemisphere associated with central regulation of sympathetic function. Collectively, our results demonstrate that blockade of brain-heart connection via alpha- and beta-adrenergic blockers significantly prolonged the detectable activities of both the heart and the brain in asphyxic rat. The beneficial effects of combined alpha and beta blockers may help extend the survival of cardiac arrest patients.http://journal.frontiersin.org/article/10.3389/fphys.2018.00099/fullatenololphentolamineautonomic nervous systemcoherencedirectional connectivityasphyxic cardiac arrest |