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Am. J. Respir. Crit. Care Med., Volume 158, Number 3, September 1998, 706-712

Pulmonary Surfactant Activity Is Impaired in Lung Transplant Recipients

JENS MICHAEL HOHLFELD, EZGI TIRYAKI, HINRICH HAMM, HEINZ GERD HOYMANN, NORBERT KRUG, AXEL HAVERICH, and HELMUT FABEL

Departments of Respiratory Medicine and Cardiothoracic Surgery, Hannover Medical School; Fraunhofer Institute of Toxicology and Aerosol Research, Hannover; and Department of Respiratory Medicine, Albert-Ludwigs-University, Freiburg, Germany

Impaired graft function in the postoperative course after lung transplantation (LTx) may in part be due to alterations in pulmonary surfactant. Animal data provide increasing evidence for surfactant abnormalities in the early course after graft reperfusion. However, little is known about the integrity of the surfactant system in human lung transplant recipients. We therefore investigated surfactant properties in bronchoalveolar lavage fluid (BALF) of patients with lung transplants (n = 60) in comparison to that of healthy subjects (n = 10). The phospholipid concentrations of BALF and of surfactant subfractions were measured, and total protein was analyzed. Surface activity was measured with a pulsating bubble surfactometer (PBS). Minimum surface tension was 15.8 ± 1.1 mN/m in lung transplant recipients, whereas healthy subjects had minimum surface tensions of 3.4 ± 1.9 mN/m (p = 0.0004). As a marker for potential surfactant inhibition, protein-to-phospholipid (PL) ratios showed no significant differences in the two major study groups. The ratio of small surfactant aggregates to large surfactant aggregates was increased in patients with lung transplants (p = 0.043). Episodes of infection or rejection did not change surface activities, nor did they induce altered ratios of protein to PL or of small to large surfactant aggregates. Surfactant activity did not correlate with pulmonary-function data. Moreover, surface tension showed no correlation with the time after transplantation. Our results suggest a persistent impairment of biophysical surfactant properties after LTx, possibly due to type-II-cell malfunction.




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