Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons

K. S. Meredith, R. A. DeLemos, J. J. Coalson, R. J. King, D. R. Gerstmann, R. Kumar, T. J. Kuehl, D. C. Winter, A. Taylor, R. H. Clark, Donald Null

Research output: Contribution to journalArticle

185 Citations (Scopus)

Abstract

To test the hypothesis that hyaline membrane disease (HMD) has a multifactorial etiology in which barotrauma plays a major role, we compared the immediate institution of high-frequency oscillatory ventilation (HFOV; 15 Hz, n = 5) with positive-pressure ventilation with positive end-expiratory pressure (PPV; n = 5) in premature baboons (140-days gestation) with HMD. Measurements of ventilation settings and physiological parameters were obtained and arterial-to-alveolar O2 (Pa(O2)-to-PA(O2)) ratio and oxygenation index [(Pa(O2/PA(O2))-to-mean airway pressure ratio (IO2)] were calculated. At death (24 h), static pressure-volume (PV) curves were performed, and phospholipids (PL) and platelet-activating factor (PAF) were measured in lung lavage fluid. Morphological inflation patterns were analyzed using a panel of standards. By design, mean airway pressure was initially higher (19 vs. 13 cmH2O) in the HFOV animals. Pa(O2)-to-PA(O2) ratio and IO2 progressively deteriorated in the PPV animals and then stabilized at significantly lower levels than with HFOV. PV curves from HFOV animals had significant increases in lung volume at maximum distending pressure, deflation volume at 10 cmH2O, and hysteresis area compared with PPV, which showed no hysteresis. Seven of seven PPV and only one of five HFOV animals had moprhological findings of HMD. PL amount and composition in both groups were consistent with immaturity, even though the quantity was significantly greater in the PPV group. PAF was present (≥ 0.10 pmol) in six of seven PPV and in the only HFOV animal with HMD. We conclude that HFOV protected PL-deficient premature baboons from changes in gas exchange, lung mechanics, and morphology typical of HMD in this model. These differences were independent of changes in PL, but the development of HMD was associated with the presence of PAF. The pathogenesis of HMD is complex and is in part related to additive lung injury.

Original languageEnglish (US)
Pages (from-to)2150-2158
Number of pages9
JournalJournal of Applied Physiology
Volume66
Issue number5
StatePublished - Jan 1 1989
Externally publishedYes

Fingerprint

Hyaline Membrane Disease
Papio
Lung Injury
Platelet Activating Factor
Phospholipids
Pressure
Positive-Pressure Respiration
Barotrauma
High-Frequency Ventilation
Lung
Economic Inflation
Bronchoalveolar Lavage Fluid
Mechanics
Ventilation
Gases
Pregnancy

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Meredith, K. S., DeLemos, R. A., Coalson, J. J., King, R. J., Gerstmann, D. R., Kumar, R., ... Null, D. (1989). Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons. Journal of Applied Physiology, 66(5), 2150-2158.

Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons. / Meredith, K. S.; DeLemos, R. A.; Coalson, J. J.; King, R. J.; Gerstmann, D. R.; Kumar, R.; Kuehl, T. J.; Winter, D. C.; Taylor, A.; Clark, R. H.; Null, Donald.

In: Journal of Applied Physiology, Vol. 66, No. 5, 01.01.1989, p. 2150-2158.

Research output: Contribution to journalArticle

Meredith, KS, DeLemos, RA, Coalson, JJ, King, RJ, Gerstmann, DR, Kumar, R, Kuehl, TJ, Winter, DC, Taylor, A, Clark, RH & Null, D 1989, 'Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons', Journal of Applied Physiology, vol. 66, no. 5, pp. 2150-2158.
Meredith KS, DeLemos RA, Coalson JJ, King RJ, Gerstmann DR, Kumar R et al. Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons. Journal of Applied Physiology. 1989 Jan 1;66(5):2150-2158.
Meredith, K. S. ; DeLemos, R. A. ; Coalson, J. J. ; King, R. J. ; Gerstmann, D. R. ; Kumar, R. ; Kuehl, T. J. ; Winter, D. C. ; Taylor, A. ; Clark, R. H. ; Null, Donald. / Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons. In: Journal of Applied Physiology. 1989 ; Vol. 66, No. 5. pp. 2150-2158.
@article{6c8c7b85caf142fba3991d896f03ece6,
title = "Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons",
abstract = "To test the hypothesis that hyaline membrane disease (HMD) has a multifactorial etiology in which barotrauma plays a major role, we compared the immediate institution of high-frequency oscillatory ventilation (HFOV; 15 Hz, n = 5) with positive-pressure ventilation with positive end-expiratory pressure (PPV; n = 5) in premature baboons (140-days gestation) with HMD. Measurements of ventilation settings and physiological parameters were obtained and arterial-to-alveolar O2 (Pa(O2)-to-PA(O2)) ratio and oxygenation index [(Pa(O2/PA(O2))-to-mean airway pressure ratio (IO2)] were calculated. At death (24 h), static pressure-volume (PV) curves were performed, and phospholipids (PL) and platelet-activating factor (PAF) were measured in lung lavage fluid. Morphological inflation patterns were analyzed using a panel of standards. By design, mean airway pressure was initially higher (19 vs. 13 cmH2O) in the HFOV animals. Pa(O2)-to-PA(O2) ratio and IO2 progressively deteriorated in the PPV animals and then stabilized at significantly lower levels than with HFOV. PV curves from HFOV animals had significant increases in lung volume at maximum distending pressure, deflation volume at 10 cmH2O, and hysteresis area compared with PPV, which showed no hysteresis. Seven of seven PPV and only one of five HFOV animals had moprhological findings of HMD. PL amount and composition in both groups were consistent with immaturity, even though the quantity was significantly greater in the PPV group. PAF was present (≥ 0.10 pmol) in six of seven PPV and in the only HFOV animal with HMD. We conclude that HFOV protected PL-deficient premature baboons from changes in gas exchange, lung mechanics, and morphology typical of HMD in this model. These differences were independent of changes in PL, but the development of HMD was associated with the presence of PAF. The pathogenesis of HMD is complex and is in part related to additive lung injury.",
author = "Meredith, {K. S.} and DeLemos, {R. A.} and Coalson, {J. J.} and King, {R. J.} and Gerstmann, {D. R.} and R. Kumar and Kuehl, {T. J.} and Winter, {D. C.} and A. Taylor and Clark, {R. H.} and Donald Null",
year = "1989",
month = "1",
day = "1",
language = "English (US)",
volume = "66",
pages = "2150--2158",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Role of lung injury in the pathogenesis of hyaline membrane disease in premature baboons

AU - Meredith, K. S.

AU - DeLemos, R. A.

AU - Coalson, J. J.

AU - King, R. J.

AU - Gerstmann, D. R.

AU - Kumar, R.

AU - Kuehl, T. J.

AU - Winter, D. C.

AU - Taylor, A.

AU - Clark, R. H.

AU - Null, Donald

PY - 1989/1/1

Y1 - 1989/1/1

N2 - To test the hypothesis that hyaline membrane disease (HMD) has a multifactorial etiology in which barotrauma plays a major role, we compared the immediate institution of high-frequency oscillatory ventilation (HFOV; 15 Hz, n = 5) with positive-pressure ventilation with positive end-expiratory pressure (PPV; n = 5) in premature baboons (140-days gestation) with HMD. Measurements of ventilation settings and physiological parameters were obtained and arterial-to-alveolar O2 (Pa(O2)-to-PA(O2)) ratio and oxygenation index [(Pa(O2/PA(O2))-to-mean airway pressure ratio (IO2)] were calculated. At death (24 h), static pressure-volume (PV) curves were performed, and phospholipids (PL) and platelet-activating factor (PAF) were measured in lung lavage fluid. Morphological inflation patterns were analyzed using a panel of standards. By design, mean airway pressure was initially higher (19 vs. 13 cmH2O) in the HFOV animals. Pa(O2)-to-PA(O2) ratio and IO2 progressively deteriorated in the PPV animals and then stabilized at significantly lower levels than with HFOV. PV curves from HFOV animals had significant increases in lung volume at maximum distending pressure, deflation volume at 10 cmH2O, and hysteresis area compared with PPV, which showed no hysteresis. Seven of seven PPV and only one of five HFOV animals had moprhological findings of HMD. PL amount and composition in both groups were consistent with immaturity, even though the quantity was significantly greater in the PPV group. PAF was present (≥ 0.10 pmol) in six of seven PPV and in the only HFOV animal with HMD. We conclude that HFOV protected PL-deficient premature baboons from changes in gas exchange, lung mechanics, and morphology typical of HMD in this model. These differences were independent of changes in PL, but the development of HMD was associated with the presence of PAF. The pathogenesis of HMD is complex and is in part related to additive lung injury.

AB - To test the hypothesis that hyaline membrane disease (HMD) has a multifactorial etiology in which barotrauma plays a major role, we compared the immediate institution of high-frequency oscillatory ventilation (HFOV; 15 Hz, n = 5) with positive-pressure ventilation with positive end-expiratory pressure (PPV; n = 5) in premature baboons (140-days gestation) with HMD. Measurements of ventilation settings and physiological parameters were obtained and arterial-to-alveolar O2 (Pa(O2)-to-PA(O2)) ratio and oxygenation index [(Pa(O2/PA(O2))-to-mean airway pressure ratio (IO2)] were calculated. At death (24 h), static pressure-volume (PV) curves were performed, and phospholipids (PL) and platelet-activating factor (PAF) were measured in lung lavage fluid. Morphological inflation patterns were analyzed using a panel of standards. By design, mean airway pressure was initially higher (19 vs. 13 cmH2O) in the HFOV animals. Pa(O2)-to-PA(O2) ratio and IO2 progressively deteriorated in the PPV animals and then stabilized at significantly lower levels than with HFOV. PV curves from HFOV animals had significant increases in lung volume at maximum distending pressure, deflation volume at 10 cmH2O, and hysteresis area compared with PPV, which showed no hysteresis. Seven of seven PPV and only one of five HFOV animals had moprhological findings of HMD. PL amount and composition in both groups were consistent with immaturity, even though the quantity was significantly greater in the PPV group. PAF was present (≥ 0.10 pmol) in six of seven PPV and in the only HFOV animal with HMD. We conclude that HFOV protected PL-deficient premature baboons from changes in gas exchange, lung mechanics, and morphology typical of HMD in this model. These differences were independent of changes in PL, but the development of HMD was associated with the presence of PAF. The pathogenesis of HMD is complex and is in part related to additive lung injury.

UR - http://www.scopus.com/inward/record.url?scp=0024315084&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024315084&partnerID=8YFLogxK

M3 - Article

C2 - 2745284

AN - SCOPUS:0024315084

VL - 66

SP - 2150

EP - 2158

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 5

ER -