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Published on: February 14, 2021
Carotid Body-Mediated Chemoreflex Drive in The Setting of low and High Output Heart Failure
Rodrigo Del Rio1, David C Andrade2, Camilo Toledo2,3
1Laboratory of Cardiorespiratory Control, Department of Physiology, Pontificia Universidad Católica de Chile, Santiago, Chile. rdelrio@bio.puc.cl.
Insights
In heart failure (HF), enhanced carotid body (CB) chemoreflex is linked to reduced cardiac output, not other HF effects. This suggests low output HF specifically potentiates the CB chemoreflex.
Area of Science:
- Cardiovascular Physiology
- Respiratory Regulation
- Heart Failure Pathophysiology
Background:
- Enhanced carotid body (CB) chemoreflex function is implicated in cardiorespiratory disorders and heart failure (HF) progression.
- The precise mechanisms of CB sensitization in HF remain unclear, though blood flow alterations are suspected.
- Previous research suggests blood flow dynamics may directly influence CB function.
Purpose of the Study:
- To investigate whether the CB-mediated chemoreflex drive is enhanced specifically in low-output HF compared to high-output HF.
- To determine the role of reduced cardiac output in CB chemoreflex potentiation during HF.
- To differentiate the effects of reduced cardiac output from other HF-related pathophysiological changes on CB function.
Main Methods:
- Utilized myocardial infarcted rats (MI-CHF) as a low-output HF model and aorto-caval fistulated rats (AV-CHF) as a high-output HF model.
- Measured blood flow supply to the CB region in MI-CHF, AV-CHF, and Sham control rats.
- Assessed hypoxic ventilatory response and apnea/hypopnea incidence in all groups.
- Quantified Kruppel-like factor 2 (KLF2) expression in the CBs of MI-CHF and AV-CHF rats.
Main Results:
- Blood flow to the CB region was significantly decreased in MI-CHF rats but not in AV-CHF rats compared to controls.
- MI-CHF rats demonstrated a significantly enhanced hypoxic ventilatory response compared to AV-CHF rats.
- Apnea/hypopnea incidence increased similarly in both MI-CHF and AV-CHF groups.
- KLF2 expression was reduced in the CBs of MI-CHF rats, correlating with reduced blood flow.
Conclusions:
- Potentiation of the CB chemoreflex in HF is strongly associated with a reduction in cardiac output.
- The enhanced chemoreflex drive in HF appears primarily linked to decreased blood flow, characteristic of low-output HF.
- Other pathophysiological consequences of HF may not be the primary drivers of CB chemoreflex potentiation.
Abstract:
Enhanced carotid body (CB) chemoreflex function is strongly related to cardiorespiratory disorders and disease progression in heart failure (HF). The mechanisms underlying CB sensitization during HF are not fully understood, however previous work indicates blood flow per se can affect CB function. Then, we hypothesized that the CB-mediated chemoreflex drive will be enhanced only in low output HF but not in high output HF. Myocardial infarcted rats and aorto-caval fistulated rats were used as a low output HF model (MI-CHF) and as a high output HF model (AV-CHF), respectively. Blood flow supply to the CB region was decreased only in MI-CHF rats compared to Sham and AV-CHF rats. MI-CHF rats exhibited a significantly enhanced hypoxic ventilatory response compared to AV-CHF rats. However, apnea/hypopnea incidence was similarly increased in both MI-CHF and AV-CHF rats compared to control. Kruppel-like factor 2 expression, a flow sensitive transcription factor, was reduced in the CBs of MI-CHF rats but not in AV-CHF rats. Our results indicate that in the setting of HF, potentiation of the CB chemoreflex is strongly associated with a reduction in cardiac output and may not be related to other pathophysiological consequences of HF.
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