316 Fetal Rat Surfactant at the Onset of Air Breathing

Abstract

V5Z lL7.Specific binding of a2-adrenergic ligands f3H] clonidine and [~HIRX 781097 was observed w i t h p l a m manbrane fragments isolated from interscapular brawn adipose tissue of 7-day-old rats.Scatchard and W o l f analyses of the data and results on specific d i s p l a c m t of DI HI norepinephrine by l m wncentrations of epinephrine and yohimbine were wnsistent with the existence ill brown adipocytes of a haegeneous class of the binding sites. Campetition experiments on b t h a-agonists and a-antagonists binding were consistent with pharmacological definition of the a2-adrenoreceptor subtype. Chemical denervation by 6-hydroxydopamine resulted in a more pronounced distinction of the hu affinity states of the receptors. A tvc-slope Scatchard plot showed mean apparent I(D of 29 and 255 M for the c i a and a 2~, respectively. The maxirmm nunber of sites was scmwhat higher (0.58 pl/nq protein) than in control animals. Pre-treatment of infant rats with yohimbine (7 days of 10 mJ/kg b.w. daily) has resulted in increased specific binding of [ 3~ yohimblne prenolol seen to indicate "hybrid" characteristics. Campetition binding studies m y be interpreted in terms that toth the aand @-adrenoreceptors in brown adipocytes of infant rats are "hybrid" species which m y in fact reside within integrated protein molecules.(Supported by Canadian Medical Research Council Grant MA-7217).-. INDUCTION O F T H E M A J O R S U R F A C T A N T APOPRO-MENT. Jeanne M. Sn der and Carole R. The major apoprotein associated with lung surfactant is a 35 kDa, sialoglycoprotein with an isoelectric point (pl) of 4.5.We used antibodies directed against the major rabbit lung surfactant apoprotein to characterize the induction of this protein during rabbit fetal lung development. Proteins from homogenates of fetal lung tissue were separated by two-dimensional (2D) gel electrophoresis, transferred to nitrocellulose paper and analyzed using an immunoblot technique. A n immunoreactive apoprotein of 26 kDa, pl 4.5, was first detectable on day 24 of gestation. Based on its migration in 2D gels, the protein did not appear to contain sialic acid. The 35 kDa form of the protein was first detectable in lung homogenates from day 30 fetal rabbits. Lamellar bodies (LB), the storage form of surfactant in the type I I cell, are first observed on day 26 of gestation. L B were purified from lung tissues of fetuses of 28 and 30 days gestation and their apoproteins were analyzed using immunoblot techniques. The apoprotein associated with the purified LB was the 35 kDa form of the protein. Therefore, a post-translational modification of the 26 kDa protein, possibly the addition of sialic acid residues, may be required for the association of the surfactant apoprotein with LB in the fetal lung type II cell. Newborn offspring of streptozotocin-diabetic rats have surprisingly superior tolerance to hyperoxic exposure compared to control offspring (Fed. Res. g:298A,1984). MECHANISMS FOR SUPERIOR HYPEROXIC TOLERANCE IN NEW-By day 13 of exposure to 95-100% 02, 79% of s...