SERUM SURFACTANT PROTEIN-A LEVELS IN PATIENTS WITH ACUTE CARDIOGENIC PULMONARY-EDEMA AND ADULT-RESPIRATORY-DISTRESS-SYNDROME

被引：95

作者：

DOYLE, IR

NICHOLAS, TE

BERSTEN, AD

机构：

[1] FLINDERS MED CTR, SCH MED, INTENS CARE UNIT, BEDFORD PK, SA 5042, AUSTRALIA

[2] FLINDERS MED CTR, SCH MED, DEPT HUMAN PHYSIOL, BEDFORD PK, SA 5042, AUSTRALIA

来源：

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE | 1995年 / 152卷 / 01期

关键词：

D O I：

10.1164/ajrccm.152.1.7599839

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

Detection of alveole-capillary damage has important implications for treatment modalities in ventilated patients. Although surfactant protein-A (SP-A) is normally only found in appreciable amounts in the lung, we describe significantly elevated concentrations in the sera of patients with acute cardiogenic pulmonary edema (median, 250 ng/ml; range, 180 to 364; n = 10) and in those with the adult respiratory distress syndrome (ARDS) (median, 378 ng/ml; range, 215 to 1,378; n = 15) relative to healthy control subjects (median, 175 ng/ml; range, 123 to 248; n = 15) and ventilated patients with no cardiorespiratory disease (median, 169 ng/ml; range, 126 to 253; n = 6) (p < 0.01, in all cases). Serum SP-A was inversely related to blood oxygenation and to static respiratory system compliance both at the time of the patient's entry into the study (p < 0.005, r(s) = -0.51, n = 31; p < 0.001, r(s) = 0.82, n = 17; respectively) and during the course of admission (p < 0.001, r(s) = -0.34, n = 168; p < 0.001, r(s) = -0.50, n = 111; respectively). In addition, we describe in detail three cases of ARDS where lung function either improved, remained static, or deteriorated. We conclude that serum SP-A is an acute indicator of lung function and alveolo-capillary membrane injury.

引用

页码：307 / 317

页数：11

共 46 条

[31] Bunnell E., Pacht E.R., Oxidized glutathione is increased in the alveolar fluid of patients with the adult respiratory distress syndrome, Am. Rev. Respir. Dis., 148, pp. 1174-1178, (1993)
[32] Voss T., Eistetter H., Schafer K.P., Engel J., Macromolecular organization of natural and recombinant lung surfactant protein SP 28-36. Structural homology with the complement factor C1q, J. Mol. Biol., 201, pp. 219-227, (1988)
[33] King R.J., Simon D., Horowitz P.M., Aspects of secondary and quaternary structure of surfactant protein A from canine lung, Biochim. Biophys. Acta, 1001, pp. 294-301, (1989)
[34] Floros J., Steinbrink R., Jacobs K., Phelps D., Kriz R., Reeny M., Sultzman L., Jones S., Taeusch H.W., Frank H.A., Fritsch E.F., Isolation and characterization of cDNA clones for the 35-kD pulmonary surfactant-associated protein, J. Biol. Chem., 61, pp. 9029-9033, (1986)
[35] Benson B.J., Hawgood S., Williams M.C., Role of apoprotein and calcium ions in surfactant function, Exp. Lung. Res., 6, pp. 223-236, (1984)
[36] Young S.L., Crapo J.P., Kremer S.A., Brumley G.W., Pulmonary surfactant lipid production in oxygen-exposed rat lungs, Lab. Invest., 46, pp. 570-576, (1982)
[37] Holm B., Notter R., Siegle J., Matalon S., Pulmonary physiological and surfactant changes during injury and recovery from hyperoxia, J. Appl. Physiol., 59, pp. 1402-1409, (1985)
[38] Tahvanainen J., Hallman M., Surfactant abnormalities after endotoxin-induced lung injury in guinea-pigs, Eur. J. Respir. Dis., 71, pp. 250-258, (1987)
[39] Coalson J.J., King R.J., Winter V.T., Prihoda T.J., Anzueto A.R., Peters J.I., Johanson Jr. W.G., O<sub>2</sub>- and pneumonia-induced lung injury. I. Pathological and morphometric studies, J. Appl. Physiol., 67, pp. 346-356, (1989)
[40] Gregory T., Longmore W., Moxley M., Whitsett J., Reed C., Fowler A., Hudson L., Maunder R., Crim C., Hyers T., Surfactant chemical composition and biophysical activity in acute respiratory distress syndrome, J. Clin. Invest., 65, pp. 1976-1981, (1991)

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