Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest
http://www.pnas.org/content/early/2015/04/02/1423936112.abstract
Significance
How does the heart of a healthy individual cease to function within just a few minutes in the absence of oxygen? We addressed this issue by simultaneously examining the heart and the brain in animal models during asphyxiation and found that asphyxia markedly stimulates neurophysiological and neurochemical activities of the brain. Furthermore, previously unidentified corticocardiac coupling showed increased intensity as the heart deteriorated. Blocking efferent input to the heart markedly increased survival time of both the heart and the brain. The results show that targeting the brain’s outflow may be an effective strategy to delay the death of the heart and the brain from asphyxia.
Abstract
The mechanism by which the healthy heart and brain die rapidly in the absence of oxygen is not well understood. We performed continuous electrocardiography and electroencephalography in rats undergoing experimental asphyxia and analyzed cortical release of core neurotransmitters, changes in brain and heart electrical activity, and brain–heart connectivity. Asphyxia stimulates a robust and sustained increase of functional and effective cortical connectivity, an immediate increase in cortical release of a large set of neurotransmitters, and a delayed activation of corticocardiac functional and effective connectivity that persists until the onset of ventricular fibrillation. Blocking the brain’s autonomic outflow significantly delayed terminal ventricular fibrillation and lengthened the duration of detectable cortical activities despite the continued absence of oxygen. These results demonstrate that asphyxia activates a brainstorm, which accelerates premature death of the heart and the brain.
Footnotes
1To whom correspondence should be addressed. Email: borjigin@umich.edu.
Author contributions: M.M.W. and J.B. conceived the project; D.L. and J.B. planned experiments and analysis; D.L. and G.X. wrote analysis programs; D.L., F.T., G.X., and S.R. analyzed data; O.S.M. and R.T.K. conceived the high-resolution analysis of brain neurochemicals; O.S.M. and S.J.C. performed liquid chromatography-mass spectrometry analysis of brain dialysates; T.L., G.X., and A.M. constructed electrodes; T.L. performed surgical implantation of all electrodes and microdialysis probe; T.L., A.M., C.P.C., and J.B. collected electroencephalogram, electrocardiogram, and electromyogram data; O.S.M., T.L., and S.J.C. conducted cortical microdialysis and sample collection; D.L. and G.X. wrote analysis program for electrocardiomatrix construction; H.G. assisted with validation of cardiac arrhythmias; and M.M.W. and J.B. wrote the paper.
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Jimo Borjigin, PhD
http://medicine.umich.edu/dept/molecular-integrative-physiology/jimo-borjigin-phd
Dr. Jimo Borjigin Interview by Alex Tsakiris on Skeptiko
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