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
C2 - 23104695
AN - SCOPUS:84871737539
SN - 8750-7587
VL - 114
SP - 99
EP - 106
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 1
ER -