|
|
||||||||
Journal of Applied Physiology, Vol 78, Issue 5 1787-1792, Copyright © 1995 by American Physiological Society
ARTICLES |
H. S. Sekhon, J. L. Wright and W. M. Thurlbeck
Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
We studied lung growth in rats between 4 and 7 wk of age under different conditions. There were five groups, seven animals in each: 1) general controls (ambient pressure and room air, food ad libitum); 2) hypobaric normoxic [barometric pressure (PB) 410 mmHg, PO2 153 Torr]; 3) normobaric hypoxic (ambient pressure, PO2 80 Torr); 4) hypobaric hypoxic (PB 410 mmHg, PO2 80 Torr); and 5) weight-matched controls to hypobaric hypoxic. Residual volume, functional residual capacity, vital capacity, and total lung capacity grew 10-20% more in both hypoxic groups than in weight-matched and general controls. Expiratory flow rates corrected for forced vital capacity decreased, and specific airway resistance increased significantly. In addition, the ratio of forced expiratory volume in 0.1 s to %forced vital capacity, peak expiratory flow rate, and forced maximal midexpiratory flow were also lower in normobaric hypoxic animals compared with weight-matched controls. Above a transpulmonary pressure of 6 cmH2O, flows were reduced in both hypoxic groups. No differences were observed between hypobaric normoxic and general control groups for lung volume and lung function. In weight-matched animals, total lung capacity decreased but lung function remained unchanged. We conclude that accelerated lung growth in hypobaric hypoxia and normobaric hypoxia is dysanaptic. Lung growth in hypobaric hypoxia is primarily induced by low oxygen, but differences between hypobaric hypoxia and normobaric hypoxia suggest a beneficial effect of low pressure.
This article has been cited by other articles:
![]() |
C. C. W. Hsia, D. M. Dane, A. S. Estrera, H. E. Wagner, P. D. Wagner, and R. L. Johnson Jr. Shifting sources of functional limitation following extensive (70%) lung resection J Appl Physiol, April 1, 2008; 104(4): 1069 - 1079. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Wongtrakool, S. Roser-Page, H. N. Rivera, and J. Roman Nicotine alters lung branching morphogenesis through the {alpha}7 nicotinic acetylcholine receptor Am J Physiol Lung Cell Mol Physiol, September 1, 2007; 293(3): L611 - L618. [Abstract] [Full Text] [PDF] |
||||
![]() |
Mechanisms and Limits of Induced Postnatal Lung Growth Am. J. Respir. Crit. Care Med., August 1, 2004; 170(3): 319 - 343. [Full Text] [PDF] |
||||
![]() |
H. S. SEKHON, J. A. KELLER, N. L. BENOWITZ, and E. R. SPINDEL Prenatal Nicotine Exposure Alters Pulmonary Function in Newborn Rhesus Monkeys Am. J. Respir. Crit. Care Med., September 15, 2001; 164(6): 989 - 994. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |