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S Slivka

Publications and source records attributed to S Slivka.

7 recordsLinked to original sources

Hyperoxia and glucocorticoid modify retinal vessel growth and interleukin-1 receptor antagonist in newborn rabbits.

Retinopathy of prematurity (ROP) is characterized by inhibition of the growth of the retinal vessels and subsequent neovascularization. Pharmacologic doses of glucocorticoids are known to decrease growth and to suppress inflammation. The aim of the present study was to investigate whether hyperoxia and/or glucocorticoid affect the growth of the retinal vessels and the expression of the anti-inflammatory cytokine IL-1 receptor antagonist (IL-1ra). The following treatments were given to newborn rabbits during the rapid growth of retinal vessels: 1) placebo and room air (n = 14); 2) dexamethasone (Dx) at 1 mg/kg/d during d 3 to 8 and room air (n = 14); 3) placebo and 100% oxygen (d 3 to 7) (n = 14); 4) Dx and O2 (n = 16). On d 12, the eyes were studied for retinal vessel length and vascular surface area from India ink-perfused vessels. When indicated, retinas were harvested on d 7 and studied for the expression of IL-1ra mRNA using Northern blot analysis. Hyperoxia decreased the length and area of the retinal vessel complexes (p < 0.01) and induced neovascularization in three of eight animals (38%). Dx decreased the length and area (p < 0.01) and tended to increase the tortuosity of the retinal vessels. Dx did not potentiate the hyperoxia-induced suppression of retinal vessel growth and prevented the hyperoxia-induced neovascularization (p = 0.04). Hyperoxia inhibited the expression of IL-1ra mRNA, whereas Dx ameliorated the hyperoxia-induced suppression of IL-1ra. According to present results, glucocorticoid decreases the retinal vessel growth and may decrease the hyperoxia-induced neovascularization. We propose that immature and damaged retinal vessels are affected by pharmacologic dosage of glucocorticoid.

Animals↗

Recombinant human erythropoietin: possible role as an antioxidant in premature rabbits.

Iron is an important catalyst for free oxygen radicals and lipid peroxidation reactions which may play a role in the pathogenesis of several diseases in premature infants. During the early neonatal period, extracellular iron is available in excessive amounts. We hypothesized that administration of erythropoietin (EPO) mobilizes iron from plasma and inhibits iron-catalyzed reactions. To evaluate this hypothesis, recombinant human EPO (rhEPO) was administered s.c. to premature rabbits delivered at 29-d gestation: one group was kept in room air (RA) and the other in a 100% oxygen environment. Within each group, the animals were randomized to receive placebo or rhEPO at 400 or at 800 U/kg on d 0 and 2 of life. On d 3 or 4, plasma iron and iron saturation of transferrin were assessed. Lipid peroxidation was analyzed in plasma and bronchoalveolar lavage fluid (BAL). Nonsedimentable protein (NSP) and phospholipid content were measured in BAL. Erythropoiesis was evaluated in liver and bone marrow. Treatment with rhEPO decreased plasma iron, decreased iron saturation of transferrin, increased reticulocytes, and increased erythropoiesis in liver and bone marrow in both RA and hyperoxia group. Oxygen exposure increased NSP in BAL and decreased the ability of BAL to inhibit lipid peroxidation as measured by malondialdehyde (MDA) generation compared with RA exposure. In O2-exposed animals, EPO treatment increased the ability of both plasma (EPO 800) and BAL (EPO 400 and 800) to inhibit lipid peroxidation and decreased NSP in BAL (EPO 400). In addition, rhEPO treatment decreased alveolar thickening and proteinaceous exudate in the hyperoxia group. We propose that by stimulating erythropoiesis, rhEPO mobilizes non-heme iron and decreases oxidant injury that depends on the availability of transient metal.

Animals↗

Perinatal development of myoinositol uptake into lung cells: surfactant phosphatidylglycerol and phosphatidylinositol synthesis in the rabbit.

It has been proposed that the high serum myoinositol promotes fetal growth and affects development of lung surfactant. However, it is unclear how the extracellular myoinositol becomes available in specific cells and whether there are developmental differences in myoinositol uptake. In the present study the mechanisms and perinatal development of intracellular myoinositol uptake into rabbit lung cells were investigated. Lung slices, lung explants, and type II alveolar cells were used. Evidence of saturable, sodium- and energy-dependent, and of non-saturable, sodium- and energy-independent myoinositol uptake was found. The nonsaturable uptake decreased by 67% during spontaneous maturation, as studied in lung slices. Beta-methasone (0.2 mg/kg days 26.3 and 27.3, to the doe) decreased by 65% the nonsaturable myoinositol uptake in 28-day-old fetuses. However, the saturable uptake revealed only small changes during perinatal development. The effect of extracellular myoinositol on surfactant phospholipid synthesis was evaluated in lung explants from 28-day-old fetuses, cultured for 2 days. In the presence of 10(-6) M dexamethasone the concentration of extracellular myoinositol, required for half-maximal inhibition of surfactant phosphatidylglycerol incorporation was higher than in explants grown without the hormone (approximately 0.4 versus 0.2 mM). However, in the microsomal fraction the phosphatidylglycerol incorporation was always inhibited by as low as 4 microM myoinositol. Myoinositol was taken up by isolated type II cells preferably by nonsaturable mechanism. The phosphatidylglycerol incorporation was less sensitive to extracellular myoinositol in adult than in fetal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Stability of fatty acids in hyperlipoproteinemic plasma during long-term storage.

Aliquots of hyperlipoproteinemic plasma were stored at -20 degrees C in a nitrogen atmosphere with added disodium ethylenediaminetetraacetate for up to one year, to determine the stability of fatty acids in the four major lipid classes under these conditions. Assays were performed at zero time and at 2, 5, and 12 months. No uniform fatty acid change was found. Minor statistically significant changes were found in total triglyceride fatty acids and in some of the individual fatty acids in cholesterol esters, phospholipid, and free fatty acids. These minor changes could not be accounted for by plasma lipid concentrations, lipolysis, or fatty acid peroxidation. Evidently, plasma can be stored in this manner for as long as a year without substantial change in fatty acids in any of the four major lipid classes.

Adult↗

Acyl transferase activities in dog lung microsomes.

Mammalian lung has a high concentration of dipalmitoyl phosphatidylcholine and other phospholipids in which both fatty acid ester chains are saturated, as opposed to the usual asymmetric phospholipid (one saturated fatty acid and one unsaturated fatty acid). The acyl transferase system in dog lung microsomes was studied by determining the reactivities of various acyl CoA derivatives with 1-lyso-2-acyl- and 1-acyl-2-lyso-phosphatidylcholine. The 16:0 derivative had equal reactivity for both the 1- and 2-lyso positions. The 18:0 derivative also exhibited marked reactivity toward both positions, although the specific activity of the enzyme when palmitoyl CoA was used was approximately twice that compared to when stearoyl CoA was used. The 16:1 derivative showed approximately the same reactivity toward the 1-lyso position as did 16:0 but both 16:1 and 18:1 were more active with the 2-lyso position. These results suggest that acyl transferases may be important in the lung to insure that sufficient amounts of dipalmitoyl phosphatidylcholine will always be present for use in pulmonary surfactant biosynthesis. It is also conceivable that the acyl transferase system described acts on 1- and 2-lyso-palmitoyl phosphatidylcholine (produced by phospholipase hydrolysis of dipalmitoyl phosphatidylcholine) in order to produce phosphatidylcholine species needed for cellular purposes other than surfactant function.

Acyltransferases↗

Isolation, characterization, and surface chemistry of a surface-active fraction from dog lung.

A procedure is described for the isolation of a surface-active fraction from dog lung. This material meets the established criteria for pulmonary surfactant. The fraction was shown to contain lipid, protein, and carbohydrate. The predominant lipid present was dipalmitoyl phosphatidylcholine. Surface chemistry studies indicated the surface properties of the fraction could not be explained solely from a consideration of the properties of dipalmitoyl phosphatidylcholine. Electron microscopic studies demonstrated the presence of intact osmiophilic bodies as well as other myelin forms in the surface-active fraction. It is speculated that, in situ, the alveolar lining layer is similar to a structured gel.

Animals↗