Myocardial infarction with a preserved ejection fraction—the impaired function of the cardio-renal baroreflex

Language
en
Document Type
Article
Issue Date
2023-04-18
First published
2023-04-04
Issue Year
2023
Authors
Pickny, Lisa
Hindermann, Martin
Ditting, Tilmann
Hilgers, Karl F.
Linz, Peter
Ott, Christian
Schmieder, Roland E.
Schiffer, Mario
Amann, Kerstin
Veelken, Roland
Editor
Publisher
Frontiers Media S.A.
Abstract

Introduction: In experimental myocardial infarction with reduced ejection fraction causing overt congestive heart failure, the control of renal sympathetic nerve activity (RSNA) by the cardio-renal baroreflex was impaired. The afferent vagal nerve activity under these experimental conditions had a lower frequency at saturation than that in controls. Hence, by investigating respective first neurons in the nodose ganglion (NG), we wanted to test the hypothesis that after myocardial infarction with still-preserved ejection fraction, the cardiac afferent nerve pathway is also already impaired.

Material and methods: A myocardial infarction was induced by coronary artery ligature. After 21 days, nodose ganglion neurons with cardiac afferents from rats with myocardial infarction were cultured. A current clamp was used to characterize neurons as “tonic,” i.e., sustained action potential (AP) firing, or “phasic,” i.e., <5 APs upon current injection. Cardiac ejection fraction was measured using echocardiography; RSNA was recorded to evaluate the sensitivity of the cardiopulmonary baroreflex. Renal and cardiac histology was studied for inflammation and fibrosis markers.

Results: A total of 192 neurons were investigated. In rats, after myocardial infarction, the number of neurons with a tonic response pattern increased compared to that in the controls (infarction vs. control: 78.6% vs. 48.5%; z-test, *p < 0.05), with augmented production of APs (23.7 ± 2.86 vs. 15.5 ± 1.86 APs/600 ms; mean ± SEM, t-test, *p < 0.05). The baseline activity of RSNA was subtly increased, and its control by the cardiopulmonary baroreflex was impaired following myocardial infarction: the fibrosis marker collagen I augmented in the renal interstitium.

Discussion: After myocardial infarction with still-preserved ejection fraction, a complex impairment of the afferent limb of the cardio-renal baroreflex caused dysregulation of renal sympathetic nerve activity with signs of renal fibrosis.

Journal Title
Frontiers in Physiology
Volume
14
Citation
Frontiers in Physiology 14 (2023): 1144620. <https://www.frontiersin.org/articles/10.3389/fphys.2023.1144620/full>
Zugehörige ORCIDs