Display options
Cite
Noly PE, Piquereau J, Coblence M, et al. Right ventricular mitochondrial respiratory function in a piglet model of chronic pulmonary hypertension. J Thorac Cardiovasc Surg. 2019;doi: 10.1016/j.jtcvs.2019.02.096.
Noly, P. E., Piquereau, J., Coblence, M., Ataam, J. A., Guihaire, J., Rucker-Martin, C., Decante, B., Haddad, F., Fadel, E., & Mercier, O. (2019). Right ventricular mitochondrial respiratory function in a piglet model of chronic pulmonary hypertension. The Journal of thoracic and cardiovascular surgery, . https://doi.org/10.1016/j.jtcvs.2019.02.096
Noly, Pierre-Emmanuel, et al. "Right ventricular mitochondrial respiratory function in a piglet model of chronic pulmonary hypertension." The Journal of thoracic and cardiovascular surgery vol. (2019). doi: https://doi.org/10.1016/j.jtcvs.2019.02.096
Noly PE, Piquereau J, Coblence M, Ataam JA, Guihaire J, Rucker-Martin C, Decante B, Haddad F, Fadel E, Mercier O. Right ventricular mitochondrial respiratory function in a piglet model of chronic pulmonary hypertension. J Thorac Cardiovasc Surg. 2019 Mar 15; doi: 10.1016/j.jtcvs.2019.02.096. Epub 2019 Mar 15. PMID: 30979421.
Copy Download .nbib Format: NLM
Share it on

J Thorac Cardiovasc Surg. 2019 Mar 15; doi: 10.1016/j.jtcvs.2019.02.096. Epub 2019 Mar 15.

Right ventricular mitochondrial respiratory function in a piglet model of chronic pulmonary hypertension.

The Journal of thoracic and cardiovascular surgery

Pierre-Emmanuel Noly, Jerôme Piquereau, Matthieu Coblence, Jennifer Arthur Ataam, Julien Guihaire, Catherine Rucker-Martin, Benoit Decante, François Haddad, Elie Fadel, Olaf Mercier

Affiliations

  1. Research and Innovation Unit, INSERM U999, DHU TORINO, Paris Sud University, Marie Lannelongue Hospital, Le Plessis Robinson, France; Department of Cardiac Surgery, Montreal Heart Institute, Montreal, Quebec, Canada. Electronic address: [email protected].
  2. UMR-S 1180, INSERM, Paris Sud University, Châtenay-Malabry, France.
  3. Research and Innovation Unit, INSERM U999, DHU TORINO, Paris Sud University, Marie Lannelongue Hospital, Le Plessis Robinson, France.
  4. Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, Calif.
  5. Research and Innovation Unit, INSERM U999, DHU TORINO, Paris Sud University, Marie Lannelongue Hospital, Le Plessis Robinson, France; Department of Thoracic and Vascular Surgery and Heart-lung Transplantation, Marie Lannelongue Hospital, Le Plessis Robinson, France.

PMID: 30979421 DOI: 10.1016/j.jtcvs.2019.02.096

Abstract

OBJECTIVE: We aimed to assess the mitochondrial respiratory capacities in the right ventricle in the setting of ventricular remodeling induced by pressure overload.

METHODS: Chronic thromboembolic pulmonary hypertension was induced in 8 piglets over a 12-week period (chronic thromboembolic pulmonary hypertension model). Right ventricular remodeling, right ventricular function, and mitochondrial respiratory function were assessed at 3, 6, and 12 weeks after induction of pulmonary hypertension and were compared with sham animals (n = 5). Right ventricular cardiomyocytes and mitochondrial structure were studied in transmission electronic microscopy after 12 weeks.

RESULTS: As of 3 weeks, chronic pressure overload induced right ventricular dilatation, right ventricular hypertrophy, and right ventricular dysfunction. Maladaptive remodeling in the chronic thromboembolic pulmonary hypertension model was confirmed by the decrease of right ventricular pulmonary artery coupling and right fractional area change. Mitochondrial functional assays in permeabilized right ventricular myocardial fibers revealed that oxidative phosphorylation capacities (complex I, complex II, and IV of the mitochondrial respiratory chain) were degraded. Furthermore, no change in substrate preference of mitochondria was found in the overloaded right ventricle. There was a good correlation between maximal mitochondrial oxygen consumption rate and right ventricular pulmonary artery coupling (Pearson coefficient r = 0.83). Transmission electronic microscopy analysis showed that the composition of cardiomyocytes was no different between the chronic thromboembolic pulmonary hypertension group and the sham group. However, mitochondrial structure anomalies were significantly increased in the chronic thromboembolic pulmonary hypertension group.

CONCLUSIONS: Mitochondrial respiratory function impairment is involved early in the development of right ventricular dysfunction in a piglet model of chronic thromboembolic pulmonary hypertension. Underlying mechanisms remain to be elucidated.

Copyright © 2019 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.

Keywords: mitochondrial metabolism; pulmonary hypertension; right ventricle

Publication Types