Supplementary Materials

Supplementary Material for:

Central-acting therapeutics alleviate respiratory weakness caused by heart failure–induced ventilatory overdrive

Andrew J. Foster, Mathew J. Platt, Jason S. Huber, Ashley L. Eadie, Alicia M. Arkell, Nadya Romanova, David C. Wright, Todd E. Gillis, Coral L. Murrant, Keith R. Brunt,* Jeremy A. Simpson*

*Corresponding author. Email: jeremys{at}uoguelph.ca (J.A.S.); keith.brunt{at}dal.ca (K.R.B.)

Published 17 May 2017, Sci. Transl. Med. 9, eaag1303 (2017)
DOI: 110.1126/scitranslmed.aag1303

This PDF file includes:

  • Fig. S1. TAC induces progressive interstitial fibrosis in the diaphragm.
  • Fig. S2. TAC induces biphasic and transient increases in diaphragm in vitro–specific force production, contractility, and passive baseline force.
  • Fig. S3. AAC induces diaphragmatic atrophy and fibrosis.
  • Fig. S4. Peripheral limb muscle CSA is unaffected in mice at 4 weeks of TAC.
  • Fig. S5. Propranolol and atenolol treatment in sham mice induces alterations in diaphragm gene expression profile.
  • Fig. S6. Propranolol and atenolol treatment in TAC mice induces alterations in diaphragm gene expression profile.
  • Table S1. TAC induces progressive changes in hemodynamics, morphometrics, and metabolic parameters throughout 18 weeks of pressure overload.
  • Table S2. Pressure overload imposed by 18 weeks of AAC induces hemodynamic and morphometric alterations similar to 9 weeks of TAC.
  • Table S3. Indices of systolic and diastolic dysfunction persist in 2-week and 4-week TAC mice treated with propranolol.

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