Decreased pulmonary compliance is an early indicator of pulmonary oxygen injury

被引:26
作者
Arkovitz, MS
Garcia, VF
Szabo, C
McConnell, K
Bove, K
Wispe, JR
机构
[1] CHILDRENS HOSP,MED CTR,DIV SURG,CINCINNATI,OH 45229
[2] CHILDRENS HOSP,MED CTR,DIV CRIT CARE MED,CINCINNATI,OH 45229
[3] CHILDRENS HOSP,MED CTR,DIV GASTROENTEROL,CINCINNATI,OH 45229
[4] CHILDRENS HOSP,MED CTR,DIV PATHOL,CINCINNATI,OH 45229
[5] CHILDRENS HOSP,MED CTR,DIV PULM BIOL,CINCINNATI,OH 45229
关键词
D O I
10.1006/jsre.1996.4980
中图分类号
R61 [外科手术学];
学科分类号
摘要
Pulmonary oxygen injury is classified by the development of tissue and alveolar edema, surfactant dysfunction, lung inflammation, and decreased pulmonary compliance. In neonates prolonged oxygen therapy is associated with the development of bronchopulmonary dysplasia. Recombinant DNA technology makes it possible to experimentally explore the role of specific proteins in the development of pulmonary oxygen injury. However, in vivo experiments require sensitive ways of identifying pulmonary oxygen injury early in its development. We therefore compared the sensitivities of several experimental assays used to assess pulmonary injury. We found that changes in pulmonary compliance were the most sensitive and showed significant differences after 72 hr of exposure to normobaric hyperoxia (FiO(2) = 0.95), which correlated with a small change in the histology of the mice lungs. The concentration of protein in the bronchoalveolar lavage fluid was less sensitive and did not differ significantly until after 96 hr of exposure. The survival in hyperoxia also did not worsen until after 96 hr. The lung wet/dry weight ratios was the least sensitive assay and did not increase until after 5 days of exposure to normobaric hyperoxia. We conclude that a decrease in pulmonary compliance is an early indicator of pulmonary oxygen injury and may be a better way to study the mechanisms and mediators of pulmonary oxygen injury. (C) 1997 Academic Press.
引用
收藏
页码:193 / 198
页数:6
相关论文
共 19 条
  • [1] Selective inhibition of the inducible isoform of nitric oxide synthase prevents pulmonary transvascular flux during acute endotoxemia
    Arkovitz, MS
    Wispe, JR
    Garcia, VF
    Szabo, C
    [J]. JOURNAL OF PEDIATRIC SURGERY, 1996, 31 (08) : 1009 - 1015
  • [2] HYPEROXIA-INDUCED ALTERATIONS OF RAT ALVEOLAR-LAVAGE COMPOSITION AND PROPERTIES
    BALAAN, MR
    BOWMAN, L
    DEDHIA, HV
    MILES, PR
    [J]. EXPERIMENTAL LUNG RESEARCH, 1995, 21 (01) : 141 - 156
  • [3] CRAPO JD, 1986, ANNU REV PHYSIOL, V48, P721
  • [4] OXYGEN-TOXICITY
    FRANK, L
    MASSARO, D
    [J]. AMERICAN JOURNAL OF MEDICINE, 1980, 69 (01) : 117 - 126
  • [5] PROTECTION FROM OXYGEN-TOXICITY WITH ENDOTOXIN - ROLE OF THE ENDOGENOUS ANTIOXIDANT ENZYMES OF THE LUNG
    FRANK, L
    SUMMERVILLE, J
    MASSARO, D
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1980, 65 (05) : 1104 - 1110
  • [6] PULMONARY PHYSIOLOGICAL AND SURFACTANT CHANGES DURING INJURY AND RECOVERY FROM HYPEROXIA
    HOLM, BA
    NOTTER, RH
    SIEGLE, J
    MATALON, S
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1985, 59 (05) : 1402 - 1409
  • [7] Jenkinson S G, 1993, New Horiz, V1, P504
  • [8] PENTOXIFYLLINE ATTENUATES OXYGEN-INDUCED LUNG INJURY
    LINDSEY, HJ
    KISALA, JM
    AYALA, A
    LEHMAN, D
    HERDON, CD
    CHAUDRY, IH
    [J]. JOURNAL OF SURGICAL RESEARCH, 1994, 56 (06) : 543 - 548
  • [9] ALTERED RESPONSES TO BACTERIAL-INFECTION AND ENDOTOXIC-SHOCK IN MICE LACKING INDUCIBLE NITRIC-OXIDE SYNTHASE
    MACMICKING, JD
    NATHAN, C
    HOM, G
    CHARTRAIN, N
    FLETCHER, DS
    TRUMBAUER, M
    STEVENS, K
    XIE, QW
    SOKOL, K
    HUTCHINSON, N
    CHEN, H
    MUDGETT, JS
    [J]. CELL, 1995, 81 (04) : 641 - 650
  • [10] Molecular medicine - Knockout mice
    Majzoub, JA
    Muglia, LJ
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1996, 334 (14) : 904 - 907