Abstract
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.
Highlights
Fatal cardiac arrest affects more than 400,000 Americans each year (Chugh et al, 2008; Stecker et al, 2014)
The data demonstrating reduced cortex-heart communication by betablocker atenolol during the later phase (Figures 7, 9) supports the hypothesis #2. These data suggest that the rapid death by asphyxia is mediated by the overstimulation of the sympathetic system of the brain
Our data in this study provide evidence for the existence of the afferent branch of the corticocardiac loop (CCL): blocking adrenergic receptors of the heart with drugs that do not penetrate the blood-brain barrier can powerfully alter the functional dynamics of cortical and corticocardiac connectivity
Summary
Fatal cardiac arrest affects more than 400,000 Americans each year (Chugh et al, 2008; Stecker et al, 2014). Past studies have shown that experimental cardiac arrest stimulates excessive neural release of catecholamines leading to fatal ventricular arrhythmias (Foley et al, 1987; Borovsky et al, 1998; Dhalla et al, 2010). Consistent with these reports, a marked surge of cardiac sympathetic activity was reported in patients with sustained ventricular arrhythmias (Meredith et al, 1991). These data demonstrate that increased cardiac sympathetic activity is causally linked with cardiac failures (Samuels, 2007; Taggart et al, 2011; Silvani et al, 2016)
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