Impaired cardiac and peripheral hemodynamic responses to inhaled β₂-agonist in cystic fibrosis

Persistent Link:
http://hdl.handle.net/10150/610329
Title:
Impaired cardiac and peripheral hemodynamic responses to inhaled β₂-agonist in cystic fibrosis
Author:
Van Iterson, E. H.; Karpen, S. R.; Baker, S. E.; Wheatley, C. M.; Morgan, W. J.; Snyder, E. M.
Affiliation:
School of Kinesiology, University of Minnesota; College of Pharmacy, University of Arizona; Department of Anesthesiology, Mayo Clinic; Department of Cardiovascular Diseases, Mayo Clinic; Department of Pediatrics, University of Arizona
Issue Date:
2015
Publisher:
BioMed Central
Citation:
Van Iterson et al. Respiratory Research (2015) 16:103 DOI 10.1186/s12931-015-0270-y
Journal:
Respiratory Research
Rights:
© 2015 Van Iterson et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/),
Collection Information:
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
Abstract:
BACKGROUND: Pulmonary system dysfunction is a hallmark of cystic fibrosis (CF) disease. In addition to impaired cystic fibrosis transmembrane conductance regulator protein, dysfunctional β2-adrenergic receptors (β2AR) contribute to low airway function in CF. Recent observations suggest CF may also be associated with impaired cardiac function that is demonstrated by attenuated cardiac output (Q), stroke volume (SV), and cardiac power (CP) at both rest and during exercise. However, β2AR regulation of cardiac and peripheral vascular tissue, in-vivo, is unknown in CF. We have previously demonstrated that the administration of an inhaled β-agonist increases SV and Q while also decreasing SVR in healthy individuals. Therefore, we aimed to assess cardiac and peripheral hemodynamic responses to the selective β2AR agonist albuterol in individuals with CF. METHODS: 18 CF and 30 control (CTL) subjects participated (ages 22 ± 2 versus 27 ± 2 and BSA = 1.7 ± 0.1 versus 1.8 ± 0.0 m2, both p < 0.05). We assessed the following at baseline and at 30- and 60-minutes following nebulized albuterol (2.5mg diluted in 3.0mL of normal saline) inhalation: 12-lead ECG for HR, manual sphygmomanometry for systolic and diastolic blood pressure (SBP and DBP, respectively), acetylene rebreathe for Q and SV. We calculated MAP = DBP + 1/3(SBP-DBP); systemic vascular resistance (SVR) = (MAP/Q)•80; CP = Q•MAP; stroke work (SW) = SV•MAP; reserve (%change baseline to 30- or 60-minutes). Hemodynamics were indexed to BSA (QI, SVI, SWI, CPI, SVRI). RESULTS: At baseline, CF demonstrated lower SV, SVI, SW, and SWI but higher HR than CTL (p < 0.05); other measures did not differ. At 30-minutes, CF demonstrated higher HR and SVRI, but lower Q, SV, SVI, CP, CPI, SW, and SWI versus CTL (p < 0.05). At 60-minutes, CF demonstrated higher HR, SVR, and SVRI, whereas all cardiac hemodynamics were lower than CTL (p < 0.05). Reserves of CP, SW, and SVR were lower in CF versus CTL at both 30 and 60-minutes (p < 0.05). CONCLUSIONS: Cardiac and peripheral hemodynamic responsiveness to acute β2AR stimulation via albuterol is attenuated in individuals with CF, suggesting β2AR located in cardiac and peripheral vascular tissue may be dysfunctional in this population.
EISSN:
1465-993X
PubMed ID:
26341519
PubMed Central ID:
PMC4560914
DOI:
10.1186/s12931-015-0270-y [doi]
Version:
Final published version
Additional Links:
http://www.respiratory-research.com/content/16/1/103

Full metadata record

DC FieldValue Language
dc.contributor.authorVan Iterson, E. H.en
dc.contributor.authorKarpen, S. R.en
dc.contributor.authorBaker, S. E.en
dc.contributor.authorWheatley, C. M.en
dc.contributor.authorMorgan, W. J.en
dc.contributor.authorSnyder, E. M.en
dc.date.accessioned2016-05-20T09:04:21Z-
dc.date.available2016-05-20T09:04:21Z-
dc.date.issued2015en
dc.identifier.citationVan Iterson et al. Respiratory Research (2015) 16:103 DOI 10.1186/s12931-015-0270-yen
dc.identifier.pmid26341519en
dc.identifier.doi10.1186/s12931-015-0270-y [doi]en
dc.identifier.urihttp://hdl.handle.net/10150/610329-
dc.description.abstractBACKGROUND: Pulmonary system dysfunction is a hallmark of cystic fibrosis (CF) disease. In addition to impaired cystic fibrosis transmembrane conductance regulator protein, dysfunctional β2-adrenergic receptors (β2AR) contribute to low airway function in CF. Recent observations suggest CF may also be associated with impaired cardiac function that is demonstrated by attenuated cardiac output (Q), stroke volume (SV), and cardiac power (CP) at both rest and during exercise. However, β2AR regulation of cardiac and peripheral vascular tissue, in-vivo, is unknown in CF. We have previously demonstrated that the administration of an inhaled β-agonist increases SV and Q while also decreasing SVR in healthy individuals. Therefore, we aimed to assess cardiac and peripheral hemodynamic responses to the selective β2AR agonist albuterol in individuals with CF. METHODS: 18 CF and 30 control (CTL) subjects participated (ages 22 ± 2 versus 27 ± 2 and BSA = 1.7 ± 0.1 versus 1.8 ± 0.0 m2, both p < 0.05). We assessed the following at baseline and at 30- and 60-minutes following nebulized albuterol (2.5mg diluted in 3.0mL of normal saline) inhalation: 12-lead ECG for HR, manual sphygmomanometry for systolic and diastolic blood pressure (SBP and DBP, respectively), acetylene rebreathe for Q and SV. We calculated MAP = DBP + 1/3(SBP-DBP); systemic vascular resistance (SVR) = (MAP/Q)•80; CP = Q•MAP; stroke work (SW) = SV•MAP; reserve (%change baseline to 30- or 60-minutes). Hemodynamics were indexed to BSA (QI, SVI, SWI, CPI, SVRI). RESULTS: At baseline, CF demonstrated lower SV, SVI, SW, and SWI but higher HR than CTL (p < 0.05); other measures did not differ. At 30-minutes, CF demonstrated higher HR and SVRI, but lower Q, SV, SVI, CP, CPI, SW, and SWI versus CTL (p < 0.05). At 60-minutes, CF demonstrated higher HR, SVR, and SVRI, whereas all cardiac hemodynamics were lower than CTL (p < 0.05). Reserves of CP, SW, and SVR were lower in CF versus CTL at both 30 and 60-minutes (p < 0.05). CONCLUSIONS: Cardiac and peripheral hemodynamic responsiveness to acute β2AR stimulation via albuterol is attenuated in individuals with CF, suggesting β2AR located in cardiac and peripheral vascular tissue may be dysfunctional in this population.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.respiratory-research.com/content/16/1/103en
dc.rights© 2015 Van Iterson et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/),en
dc.titleImpaired cardiac and peripheral hemodynamic responses to inhaled β₂-agonist in cystic fibrosisen
dc.typeArticleen
dc.identifier.eissn1465-993Xen
dc.contributor.departmentSchool of Kinesiology, University of Minnesotaen
dc.contributor.departmentCollege of Pharmacy, University of Arizonaen
dc.contributor.departmentDepartment of Anesthesiology, Mayo Clinicen
dc.contributor.departmentDepartment of Cardiovascular Diseases, Mayo Clinicen
dc.contributor.departmentDepartment of Pediatrics, University of Arizonaen
dc.identifier.journalRespiratory Researchen
dc.identifier.pmcidPMC4560914en
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen

Related articles on PubMed

All Items in UA Campus Repository are protected by copyright, with all rights reserved, unless otherwise indicated.