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The use of exogenous surfactants has been introduced into the therapy of patients of different ages. Much better results have been obtained in the treatment of respiratory distress syndrome with surfactants enriched with surfactant proteins. In the following study we used protein-containing surfactants (survanta and curosurf). The aim of the following study was to determine the localisation of artificial surfactants in the lung tissue. Using the Immunogold Technique, biotinylated surfactant proteins were traced in the air-blood barriers. In all lungs the exogenous surfactant was present only in some alveoli. In these parts small areas of atelectasis as well as oedema and transudate accumulation were seen. These changes were less severe after biotinylated curosurf treatment. In electron microscope studies we found surfactant elements in the air-blood barrier and other structures of the alveolar septa. Immunogold studies confirm the presence of biotynylated surfactant in the elements of the air-blood barrier.

Treatment of pre-term newborns with exogenous surfactant preparation is a well established part of the therapy for respiratory distress syndrome of the newborns (RDS). Since the introduction of surfactant into clinical practice in 1980, hundreds of studies have been published describing beneficial effects of such treatment. There is only limited number of morphological publications reporting adverse effects of surfactant administration. The aim of the present study is to describe morphological changes in the lung after surfactant administration to healthy newborn rats. Two types of surfactant were used: Exosurf (Glaxo Wellcome, England) and Survanta (Abbott Laboratories, USA). Surfactant preparation were given intratracheally in single dose (bolus) (100 mg of lipids per kg b.w.). Animals from control group received 0.9% saline in equivalent volume. Lung specimens were taken 15, 20, 25 and 30 minutes after drug administration and evaluated by light and electron microscopy. There was no damage in lungs from the control group. Tissue specimens from the Exosurf group revealed severe pathological changes: foci of atelectasis, frank edema in the parenchyma, focal disruption of air-blood barrier, hemorrhages in many alveoli, surfactant particles in many alveolar capillaries, and strongly activated alveolar macrophages. In this group changes appeared as early as 15 min after surfactant administration and intensity of lung injury increased with time. Also, Survanta administration caused damage to the lung tissue. However, the changes were less intense and appeared later (20-25 minutes after Survanta treatment). In conclusion, the presented morphological findings proved that exogenous surfactant administration to healthy rat newborns caused lung damage. Comparing two different surfactant preparation, Exosurf and Survanta, it was shown that the former one produced stronger and faster damage to lung alveoli than the latter one.

The goal of the present study was to elucidate the migration of surfactant-like material into the alveolar capillaries of newborn rats. The lungs of experimental animals were studied by ultrastructural techniques-standard electron microscopy as well as immunoelectron microscopy-using antibodies against synthetic polypeptide complementary to the noncollagenous part of surfactant protein A (SP-A). Antibodies exhibited specific reaction with native rat SP-A in Western blot and immunohistochemical analysis. Surfactant was observed in the alveolar space, type II pneumocytes, macrophages, type I pneumocytes, endothelial cells, the extracellular space of the alveolar septa and in the alveolar capillaries. Lamellar structures observed in all elements of the blood-air barrier as well as in the alveolar capillaries were stained positively with anti-SP-A antibodies. Transport of the pulmonary surfactant into the circulatory system was observed more frequently during the first 6-8 h of extrauterine life of newborn rats, although it was also seen in the blood vessels till 48 h after delivery. The results of our investigation suggest that clearance of surfactant via the circulatory system plays an important role in the early postnatal period.

In newborn rats we investigated the entrance of surfactant to the pulmonary capillaries a few minutes after the birth. Time is crucial for the process which can be called "drying" of the lung, when a large amount of intraalveolar fluid enters the pulmonary circulation. Ultrastructural studies have revealed bulk transport and endocytosis of surfactant via alveolar septa to the blood vessels, but it is still questionable whether the entrance of surfactant to pulmonary capillaries is related to its clearance or to "drying" of lung's alveoli.