Separating in vivo mechanical stimuli for postpneumonectomy compensation

Physiological assessment

D. Merrill Dane, Cuneyt Yilmaz, Aaron S. Estrera, Connie C W Hsia

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Separating in vivo mechanical stimuli for postpneumonectomy compensation: physiological assessment. J Appl Physiol 114: 99-106, 2013. First published October 25, 2012; doi:10.1152/japplphysiol.01213.2012.-Following right pneumonectomy (PNX), the remaining lung expands and its perfusion doubles. Tissue and microvascular mechanical stresses are putative stimuli for initiating compensatory lung growth and remodeling, but their relative contributions to overall compensation remain uncertain. To temporally isolate the stimuli related to post-PNX lung expansion (parenchyma deformation) from those related to the sustained increase in perfusion (microvascular distention and shear), we replaced the right lung of adult dogs with a custom-shaped inflated prosthesis. Following stabilization of perfusion and wound healing 4 mo later, the prosthesis was either acutely deflated (DEF group) or kept inflated (INF group). Physiological studies were performed pre-PNX, 4 mo post-PNX (inflated prosthesis, INF1), and again 4 mo postdeflation (DEF) compared with controls with simultaneous INF prosthesis (INF2). Perfusion to the remaining lung increased ̃76-113% post-PNX (INF1 and INF2) and did not change postdeflation. Post-PNX (INF prosthesis) end-expiratory lung volume (EELV) and lung and membrane diffusing capacities (DLCO and DMCO) at a given perfusion were 25-40% below pre-PNX baseline. In the INF group EELV, DLCO and DMCO remained stable or declined slightly with time. In contrast, all of these parameters increased significantly after deflation and were 157%, 26%, and 47%, respectively, above the corresponding control values (INF2). Following delayed deflation, lung expansion accounted for 44%-48% of total post-PNX compensatory increase in exercise DLCO and peak O2 uptake; the remainder fraction is likely attributable to the increase in perfusion. Results suggest that expansion-related parenchyma mechanical stress and perfusion-related microvascular stress contribute in equal proportions to post-PNX alveolar growth and remodeling.

Original languageEnglish (US)
Pages (from-to)99-106
Number of pages8
JournalJournal of Applied Physiology
Volume114
Issue number1
DOIs
StatePublished - Jan 1 2013

Fingerprint

Lung
Perfusion
Prostheses and Implants
Mechanical Stress
Pneumonectomy
Growth
Wound Healing
Dogs
Membranes
butyl phosphorotrithioate

Keywords

  • Lung diffusing capacity
  • Lung resection
  • Mechanical deformation
  • Mechanical signals
  • Pulmonary perfusion

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Separating in vivo mechanical stimuli for postpneumonectomy compensation : Physiological assessment. / Dane, D. Merrill; Yilmaz, Cuneyt; Estrera, Aaron S.; Hsia, Connie C W.

In: Journal of Applied Physiology, Vol. 114, No. 1, 01.01.2013, p. 99-106.

Research output: Contribution to journalArticle

Dane, D. Merrill ; Yilmaz, Cuneyt ; Estrera, Aaron S. ; Hsia, Connie C W. / Separating in vivo mechanical stimuli for postpneumonectomy compensation : Physiological assessment. In: Journal of Applied Physiology. 2013 ; Vol. 114, No. 1. pp. 99-106.
@article{50e979898fef4242be418fa724d4b133,
title = "Separating in vivo mechanical stimuli for postpneumonectomy compensation: Physiological assessment",
abstract = "Separating in vivo mechanical stimuli for postpneumonectomy compensation: physiological assessment. J Appl Physiol 114: 99-106, 2013. First published October 25, 2012; doi:10.1152/japplphysiol.01213.2012.-Following right pneumonectomy (PNX), the remaining lung expands and its perfusion doubles. Tissue and microvascular mechanical stresses are putative stimuli for initiating compensatory lung growth and remodeling, but their relative contributions to overall compensation remain uncertain. To temporally isolate the stimuli related to post-PNX lung expansion (parenchyma deformation) from those related to the sustained increase in perfusion (microvascular distention and shear), we replaced the right lung of adult dogs with a custom-shaped inflated prosthesis. Following stabilization of perfusion and wound healing 4 mo later, the prosthesis was either acutely deflated (DEF group) or kept inflated (INF group). Physiological studies were performed pre-PNX, 4 mo post-PNX (inflated prosthesis, INF1), and again 4 mo postdeflation (DEF) compared with controls with simultaneous INF prosthesis (INF2). Perfusion to the remaining lung increased ̃76-113{\%} post-PNX (INF1 and INF2) and did not change postdeflation. Post-PNX (INF prosthesis) end-expiratory lung volume (EELV) and lung and membrane diffusing capacities (DLCO and DMCO) at a given perfusion were 25-40{\%} below pre-PNX baseline. In the INF group EELV, DLCO and DMCO remained stable or declined slightly with time. In contrast, all of these parameters increased significantly after deflation and were 157{\%}, 26{\%}, and 47{\%}, respectively, above the corresponding control values (INF2). Following delayed deflation, lung expansion accounted for 44{\%}-48{\%} of total post-PNX compensatory increase in exercise DLCO and peak O2 uptake; the remainder fraction is likely attributable to the increase in perfusion. Results suggest that expansion-related parenchyma mechanical stress and perfusion-related microvascular stress contribute in equal proportions to post-PNX alveolar growth and remodeling.",
keywords = "Lung diffusing capacity, Lung resection, Mechanical deformation, Mechanical signals, Pulmonary perfusion",
author = "Dane, {D. Merrill} and Cuneyt Yilmaz and Estrera, {Aaron S.} and Hsia, {Connie C W}",
year = "2013",
month = "1",
day = "1",
doi = "10.1152/japplphysiol.01213.2012",
language = "English (US)",
volume = "114",
pages = "99--106",
journal = "Journal of Applied Physiology",
issn = "0161-7567",
publisher = "American Physiological Society",
number = "1",

}

TY - JOUR

T1 - Separating in vivo mechanical stimuli for postpneumonectomy compensation

T2 - Physiological assessment

AU - Dane, D. Merrill

AU - Yilmaz, Cuneyt

AU - Estrera, Aaron S.

AU - Hsia, Connie C W

PY - 2013/1/1

Y1 - 2013/1/1

N2 - Separating in vivo mechanical stimuli for postpneumonectomy compensation: physiological assessment. J Appl Physiol 114: 99-106, 2013. First published October 25, 2012; doi:10.1152/japplphysiol.01213.2012.-Following right pneumonectomy (PNX), the remaining lung expands and its perfusion doubles. Tissue and microvascular mechanical stresses are putative stimuli for initiating compensatory lung growth and remodeling, but their relative contributions to overall compensation remain uncertain. To temporally isolate the stimuli related to post-PNX lung expansion (parenchyma deformation) from those related to the sustained increase in perfusion (microvascular distention and shear), we replaced the right lung of adult dogs with a custom-shaped inflated prosthesis. Following stabilization of perfusion and wound healing 4 mo later, the prosthesis was either acutely deflated (DEF group) or kept inflated (INF group). Physiological studies were performed pre-PNX, 4 mo post-PNX (inflated prosthesis, INF1), and again 4 mo postdeflation (DEF) compared with controls with simultaneous INF prosthesis (INF2). Perfusion to the remaining lung increased ̃76-113% post-PNX (INF1 and INF2) and did not change postdeflation. Post-PNX (INF prosthesis) end-expiratory lung volume (EELV) and lung and membrane diffusing capacities (DLCO and DMCO) at a given perfusion were 25-40% below pre-PNX baseline. In the INF group EELV, DLCO and DMCO remained stable or declined slightly with time. In contrast, all of these parameters increased significantly after deflation and were 157%, 26%, and 47%, respectively, above the corresponding control values (INF2). Following delayed deflation, lung expansion accounted for 44%-48% of total post-PNX compensatory increase in exercise DLCO and peak O2 uptake; the remainder fraction is likely attributable to the increase in perfusion. Results suggest that expansion-related parenchyma mechanical stress and perfusion-related microvascular stress contribute in equal proportions to post-PNX alveolar growth and remodeling.

AB - Separating in vivo mechanical stimuli for postpneumonectomy compensation: physiological assessment. J Appl Physiol 114: 99-106, 2013. First published October 25, 2012; doi:10.1152/japplphysiol.01213.2012.-Following right pneumonectomy (PNX), the remaining lung expands and its perfusion doubles. Tissue and microvascular mechanical stresses are putative stimuli for initiating compensatory lung growth and remodeling, but their relative contributions to overall compensation remain uncertain. To temporally isolate the stimuli related to post-PNX lung expansion (parenchyma deformation) from those related to the sustained increase in perfusion (microvascular distention and shear), we replaced the right lung of adult dogs with a custom-shaped inflated prosthesis. Following stabilization of perfusion and wound healing 4 mo later, the prosthesis was either acutely deflated (DEF group) or kept inflated (INF group). Physiological studies were performed pre-PNX, 4 mo post-PNX (inflated prosthesis, INF1), and again 4 mo postdeflation (DEF) compared with controls with simultaneous INF prosthesis (INF2). Perfusion to the remaining lung increased ̃76-113% post-PNX (INF1 and INF2) and did not change postdeflation. Post-PNX (INF prosthesis) end-expiratory lung volume (EELV) and lung and membrane diffusing capacities (DLCO and DMCO) at a given perfusion were 25-40% below pre-PNX baseline. In the INF group EELV, DLCO and DMCO remained stable or declined slightly with time. In contrast, all of these parameters increased significantly after deflation and were 157%, 26%, and 47%, respectively, above the corresponding control values (INF2). Following delayed deflation, lung expansion accounted for 44%-48% of total post-PNX compensatory increase in exercise DLCO and peak O2 uptake; the remainder fraction is likely attributable to the increase in perfusion. Results suggest that expansion-related parenchyma mechanical stress and perfusion-related microvascular stress contribute in equal proportions to post-PNX alveolar growth and remodeling.

KW - Lung diffusing capacity

KW - Lung resection

KW - Mechanical deformation

KW - Mechanical signals

KW - Pulmonary perfusion

UR - http://www.scopus.com/inward/record.url?scp=84871737539&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84871737539&partnerID=8YFLogxK

U2 - 10.1152/japplphysiol.01213.2012

DO - 10.1152/japplphysiol.01213.2012

M3 - Article

VL - 114

SP - 99

EP - 106

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 0161-7567

IS - 1

ER -