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At least 757 records · Page 42Linked to original sources
PubMed2001

Effects of mannitol on the acute lung injury induced by oleic acid in rats.

Our purpose was to evaluate the pulmonary effects of mannitol infusion in a rat model of acute lung injury induced by oleic acid (OA) to compare the effects of mannitol to those of another diuretic, furosemide (FUR), and to assess if mannitol effects remained after correction of the volume depletion induced by this agent. Acute lung injury was induced in Wistar rats by intravenous administration of 100 mg/kg of OA. Mannitol (1 mL of a 20% solution) was infused either 15 min before or 2 h after OA infusion. FUR was infused intravenously in a dose (1 mg/kg) that induced a similar amount of diuresis compared to mannitol. We also studied rats that received NaCl 0.9% infusion to correct for volume losses induced by mannitol. The severity of the acute lung injury was evaluated by morphometric studies of the lungs 4 h after OA infusion. The amount of intraalveolar fluid accumulation and the intensity of alveolar distention and collapse were evaluated. Mannitol infusion either 15 min before or 2 h after OA administration resulted in a significant decrease in the amount of intraalveolar edema and alveolar distention and collapse (P < 0.001). FUR administration before OA infusion had an effect similar to mannitol. We did not observe any significant effect of mannitol when the rats received saline infusion to correct for diuresis induced by mannitol. We conclude that mannitol decreases the severity of pulmonary injury induced by OA in rats. This effect is mainly due to its diuretic properties.

Animals↗
PubMed1997

Effects of oleic acid lung injury and positive end-expiratory pressure on central hemodynamics and regional blood flow.

The objective of our study was to investigate the influence on central and regional circulation of the application of positive end-expiratory pressure (PEEP=P) in a canine model of low hydrostatic pulmonary edema. Eight mongrel dogs with oleic acid-induced pulmonary edema were artificially ventilated with and without PEEP. Regional blood flow was determined using radioactive microspheres directly injected into the left ventricle. Regional blood flow to the brain was maintained under all experimental conditions, while the blood flow to the gastric fundal mucosa and to the pancreas significantly decreased following PEEP, oleic acid injection (OA) and with PEEP and oleic acid combination (P+OA). The renal blood flow decreased only during the P+OA phase. We conclude that the observed decrease in blood flow to the gastrointestinal mucosa and renal circulation in this acute low hydrostatic pressure pulmonary edema may correlate with the increased incidence of gastrointestinal and renal complications that accompany critically ill patients.

Animals↗
PubMed1980

Effects of feeding oleic acid or hydrogenated vegetable oils to lactating cows.

In feeding trials to clarify the mechanism by which unsaturated oils depress milk fat percentage, oleic acid at 250 or 500 ml per cow per day did not reduce milk fat percentage significantly. At 500 ml these changes were significant (control, oleic): rumen acetate 61.6, 60.3%; rumen propionate 19.4, 21.0%; milk fat content of 18:1 trans fatty acid 3.0, 8.0%; and of 18:2 cis fatty acid 2.2, 1.4%. Feeding hydrogenated vegetable oil containing 13% trans acid at 454 g per cow per day decreased slightly milk fat percentage and elevated plasma cholesterol 190 to 245 mg/100 ml and 18:1 trans fatty acid in milk fat 4.2 to 6.2%. Hydrogenated vegetable oil containing 49% 18:1 trans acid at 454 g daily decreased milk fat 3.9 to 3.1%. Milk fat triglycerides decreased in short chain fatty acids and increased in 18:1 trans 2.6 to 11.2%, 18:1 cis 22.9 to 29.0%, and 18:2 trans .2 to 1.8%. Milk phospholipids decreased 14.1 to 9.6% in 14:0 fatty acid and increased .3 to 3.1% in 18:1 trans and 20.5 to 31.4% in 18:1 cis. Blood cholesterol esters were increased 152 to 195 mg/100 ml. The data lend support to the concept that trans acids or compounds produced in the rumen during their formation from polyunsaturated fatty acids are responsible for the milk fat depression from unsaturated oils.

Animals↗
PubMed2001

Effect of endotoxin on oleic acid lung injury does not depend on priming.

Recent studies have demonstrated significant synergistic physiological and biochemical effects between low-dose endotoxin (Etx) administration and oleic acid (OA)-induced canine lung injury. To evaluate whether this interaction depends on Etx priming of some key cell population, we compared the effects of giving low-dose Etx both after as well as before inducing lung injury with OA. In addition to hemodynamic and blood-gas measurements, positron emission tomographic imaging was used to measure edema accumulation and intrapulmonary blood flow distribution. Biochemical measurements of the stable metabolites of prostacyclin and thromboxane were obtained as well as measurements of isoprostanes and reactive sulfhydryls as evidence for possible concomitant oxidant production. We found that the physiological and biochemical effects of low-dose Etx developed 30-45 min after its administration, regardless of whether Etx was administered before or after OA. No increase in either isoprostane or reactive sulfhydryl production after Etx and/or OA was detected. These data suggest that the synergistic effect of low-dose Etx and OA-induced lung injury is not due to a priming effect of Etx.

Animals↗
PubMed1999

Increase in hepatic content of oleic acid induced by dehydroepiandrosterone in the rat.

The effects of dehydroepiandrosterone (DHEA) on the acyl composition of lipids in rat liver were studied. The content of oleic acid (18:1) in hepatic lipids was increased markedly by feeding rats a diet containing 0.5% (w/w) DHEA for 14 days. Treatment of rats with DHEA caused an increase in the activity of the terminal desaturase of the stearoyl-CoA desaturation system, without changing either the activity of NADH-cytochrome b5 reductase or the microsomal content of cytochrome b5. Among the changes observed in hepatic lipids, the increase in 18:1 content in phosphatidylcholine (PtdCho) was the most prominent; an approximately 2.5-fold increase in the proportion of 18:1 was induced at position 2, but not at position 1, by DHEA. This selective elevation of 18:1 at position 2 of PtdCho seems to be produced by the concerted actions of the induced 1-acylglycerophosphocholine (1-acyl-GPC) acyltransferase and the induced stearoyl-CoA desaturase. The content of 18:1 in serum lipids was unchanged by DHEA treatment, suggesting that secretion of lipids containing 18:1 into the circulation was not affected by DHEA. These results suggest that the elevation of hepatic content of 18:1 caused by DHEA treatment is mainly due to the induction of stearoyl-CoA desaturase.

Animals↗
PubMed2005

Ozonolysis of mixed oleic-acid/stearic-acid particles: reaction kinetics and chemical morphology.

The ozonolysis of mixed oleic-acid/stearic-acid (OL/SA) aerosol particles from 0/100 to 100/0 wt % composition is studied. The magnitude of the divergence of the particle beam inside an aerosol mass spectrometer shows that, in the concentration range 100/0 to 60/40, the mixed OL/SA particles are liquid prior to reaction. Upon ozonolysis, particles having compositions of 75/25 and 60/40 change shape, indicating that they have solidified during reaction. Transmission electron micrographs show that SA(s) forms needles. For particles having compositions of 75/25, 60/40, and greater SA content, the reaction kinetics exhibit an initial fast decay of OL for low O(3) exposure with no further loss of OL at higher O(3) exposures. For compositions from 50/50 to 10/90, the residual OL concentration remains at 28 +/- 2% of its initial value. The initial reactive uptake coefficient for O(3), as determined by OL loss, decreases linearly from 1.25 (+/-0.2) x 10(-3) to 0.60 (+/-0.15) x 10(-3) for composition changes of 100/0 to 60/40. At 50/50 composition, the uptake coefficient drops abruptly to 0.15 (+/-0.1) x 10(-3), and there are no further changes with increased SA content. These observations can be explained with a combination of three postulates: (1) Unreacted mixed particles remain as supersaturated liquids up to 60/40 composition, and the OL in this form rapidly reacts with O(3). (2) SA, as it solidifies, locks into its crystal structure a significant amount of OL, and this OL is completely inaccessible to O(3). (3) Accompanying crystallization, some stearic acid molecules connect as a filamentous network to form a semipermeable gel containing liquid OL but with a reduced uptake coefficient because of the decrease in molecular diffusivity in the gel. An individual particle of 50/50 to 90/10 is hypothesized as a combination of SA crystals having OL impurities (postulate 2) that are partially enveloped by an SA/OL gel (postulate 3) to explain (a) the abrupt drop in the uptake coefficient from 60/40 to 50/50 and (b) the residual OL content even after high ozone exposure. The results of this study, pointing out the important effects of particle phase, composition, and morphology on chemical reactivity, contribute to an improved understanding of the aging processes of atmospheric aerosol particles.

Journal Article↗
PubMed1998

Strain-dependent cytokine profile and susceptibility to oleic acid anilide in a murine model of the toxic oil syndrome.

The toxic oil syndrome (TOS) was caused by the ingestion of an adulterated rapeseed oil containing oleic acid anilide (OAA). It was characterized by lethal symptoms in the acute phase and by symptoms of idiopathic autoimmune diseases in the chronic phase. The pathogenetic mechanisms remain unclear. In a murine model of TOS we demonstrate strain-dependent effects on the immune system after treatment with OAA intraperitoneally. While C57BL/6 (H-2b) mice develop a polyclonal B cell activation without disease symptoms, most A/J (H-2a) mice suffer an acute lethal wasting disease. These differences are reflected in the splenic cytokine gene expression and secretion and in the Ig production. Increased IgE serum levels and reduced TNF-beta mRNA suggest a Th2 cell response in C57BL/6 mice. In A/J mice, splenocytes express IL-1alpha, IL-10, and IFN-gamma mRNA in vivo and secrete high levels of TNF-alpha in vitro. These observations resemble the human condition in TOS with development of either an acute lethal disease or a chronic autoimmune-like disease. As in other chemical-induced reactions genetic susceptibility seems to be important.

Anilides↗
PubMed2002

Strain-dependent in vitro and in vivo effects of oleic acid anilides on splenocytes and T cells in a murine model of the toxic oil syndrome.

The toxic oil syndrome is an exogenously-induced autoimmune disease in humans, which is believed to be due to the accidental ingestion of oleic acid anilides. In a previously established murine model anilides-treated A/J mice developed a wasting disease after 1 week. Anilides-treated B10.S mice showed after 6 weeks a hyperimmunglobulinemia with autoantibody production, but no clinical symptoms. We now compared in vitro the effects of anilides on splenocytes and T cells in A/J and B10.S mice. Splenocyte proliferation was similar in both strains. After in vivo treatment of mice with anilides and in vitro restimulation, splenocytes of sick A/J mice showed a significant increase in splenocyte proliferation. Splenocytes from B10.S mice, however, had a suppressed baseline response and did not proliferate on restimulation. Adherent cells were necessary to induce proliferation in A/J mice-derived T cells. Apoptosis in splenocytes was significantly elevated in anilides-treated A/J and in B10.S mice as compared to saline-treated controls. These data show that anilides are able to affect the immune system in a strain-dependent way and may therefore take part in inducing the disease seen in humans and mice.

Anilides↗