Arterial Chemoreflex Protective Effect on Left Ventricle Energetics and Changes after Myocardial Infarct

Abstract

The Arterial Chemoreflex negative feedback mechanism regulates the cardiovascular responses to arterial oxygen and carbon dioxide concentrations as sensed by carotid chemoreceptors. Whenever the arterial pressure of oxygen chnages the Autonomic Nervous System madulates heart rate and arterial blood pressure. As the Arterial Chemoreflex influences cardiac output to compensate for changes in oxygen arterial pressure, we hypothesized that it must influence the mechanical interaction between the left ventricle and the arterial tree, as well as cardiac energy consumption and efficiency during Myocardial Infarct. The Arterial Chemoreflex was provoked by the application of lobeline in the left-carotid sinus of 11 rabbits anesthetized, paralyzed and artificially ventilated; an intraventricular impedance catheter was used to measure simultaneously ventricular pressure and volume. All experiments were performed according to national laws and international guidelines. We designed a custom software to compute beat by beat left-ventricle end-systolic elastance (Ees), arterial elastance (Ea) and the ventriculo arteral coupling ratio (Ea/Ees); from this data we calculated left-ventricular stroke work (SW), total energy expenditure (PVA), ratio of the SW to its theoretical maximum (Qload) and cardiac energetic efficiency (CEE=SW/PVA). Under Basal Conditions and after Myocardial Infarct the Arterial Chemoreflex increased Ees and Ea in paralell, without any change in Ees/Ea. SW and PVA both decreased, without any change of Qload or CEE (Table). Ventriculo-arterial coupling was maintained in the interval of optimal cardiac mechanical and energetic efficiency. In conclusion, the Arterial Chemoreflex is a control mechanism of the cardiovascular system that exerts a feedback modulation on cardiovascular responses through an increase in both left ventricle contractility and arterial elastance, in such a balanced way that ventriculo-arterial coupling is mantained, mechanical and energetic efficiency are maintained at optimal values. Most remarckably the increase in ventricular and arterial elastance is acomplished decreasing the SW and PVA(equivalent to myocardial oxygen demand), therefore emphasizing the protective effect of the Arterial Chemoreflex the myocardial oxygen comnsumption is ischemic conditions. Support or Funding Information PHYSIOMAT - Modelação Matemática e Computacional da Fisiologia Humana (2013) Fundação para a Ciência e Tecnologia EXCL/MAT-NAN/0114/2012 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.