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Baroreflex Influence on Left Ventricle Energetics and Changes after Myocardial Infarct
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In the classic description the Baroreflex is a negative feedback mechanism that controls arterial blood pressure, as sensed by the baroreceptors. It is a key component of the Autonomic regulation of the circulation in normal conditions and during Myocardial Infarction.
As the Baroreflex influences the heart rate, cardiac contractility and vascular resistance, we hypothesised 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 Infarction.
The Baroreflex was evaluated in 11 rabbits by partial occlusion of the common carotid artery before and after the induction of cardiac ischemia by the occlusion of the left anterior descending artery. The left ventricular pressure and left ventricular volume were measured with an intraventricular pressure and impedance catheter.
We designed a custom software to characterize beat by beat left‐ventricular and arterial physiologic properties. From this data, left‐ventricle end‐systolic elastance (Ees), arterial elastance (Ea) and the coupling ratio (Ea/Ees) were computed. We also calculated left‐ventricular stroke work (SW), total energy expenditure (PVA), mechanical efficiency measured by the ratio of the SW to its theoretical maximum (Qload) and cardiac energetic efficiency (CEE=SW/PVA).
In Basal conditions upon the application of the Baroreflex, the Ees, Ea showed an approximately similar increase which resulted in a constant Ea/Ees. SW and PVA increased while Qload and CEE remained similar. After Myocardial Infarction there is an alteration in the Baroreflex response that increases Ea and Ees differently which resulted in an increase in Ea/Ees ratio. SW and PVA increased while Qload decreased and CEE remained similar (Table). The main difference between Basal and Myocardial Infarct responses during the Baroreflex are the increase in Ea/Ees and the decrease in Qload.
In conclusion the Baroreflex is a control mechanism of the cardiovascular system which exerts a feedback modulation on the arterial pressure through a balanced increase in cardiac contractility and arterial elastance, that preserves both its mechanical and energetic efficiency in Basal conditions. After Myocardial Infarct the Baroreflex changes its behaviour and increases cardiac contractility and arterial elastance maintaining the energetic efficiency crucial during ischemia at the expense of a decrease in mechanical efficiency.
Support or Funding Information
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
.
Title: Baroreflex Influence on Left Ventricle Energetics and Changes after Myocardial Infarct
Description:
In the classic description the Baroreflex is a negative feedback mechanism that controls arterial blood pressure, as sensed by the baroreceptors.
It is a key component of the Autonomic regulation of the circulation in normal conditions and during Myocardial Infarction.
As the Baroreflex influences the heart rate, cardiac contractility and vascular resistance, we hypothesised 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 Infarction.
The Baroreflex was evaluated in 11 rabbits by partial occlusion of the common carotid artery before and after the induction of cardiac ischemia by the occlusion of the left anterior descending artery.
The left ventricular pressure and left ventricular volume were measured with an intraventricular pressure and impedance catheter.
We designed a custom software to characterize beat by beat left‐ventricular and arterial physiologic properties.
From this data, left‐ventricle end‐systolic elastance (Ees), arterial elastance (Ea) and the coupling ratio (Ea/Ees) were computed.
We also calculated left‐ventricular stroke work (SW), total energy expenditure (PVA), mechanical efficiency measured by the ratio of the SW to its theoretical maximum (Qload) and cardiac energetic efficiency (CEE=SW/PVA).
In Basal conditions upon the application of the Baroreflex, the Ees, Ea showed an approximately similar increase which resulted in a constant Ea/Ees.
SW and PVA increased while Qload and CEE remained similar.
After Myocardial Infarction there is an alteration in the Baroreflex response that increases Ea and Ees differently which resulted in an increase in Ea/Ees ratio.
SW and PVA increased while Qload decreased and CEE remained similar (Table).
The main difference between Basal and Myocardial Infarct responses during the Baroreflex are the increase in Ea/Ees and the decrease in Qload.
In conclusion the Baroreflex is a control mechanism of the cardiovascular system which exerts a feedback modulation on the arterial pressure through a balanced increase in cardiac contractility and arterial elastance, that preserves both its mechanical and energetic efficiency in Basal conditions.
After Myocardial Infarct the Baroreflex changes its behaviour and increases cardiac contractility and arterial elastance maintaining the energetic efficiency crucial during ischemia at the expense of a decrease in mechanical efficiency.
Support or Funding Information
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
.
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