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At least 235 records · Page 13Linked to original sources
PubMed1998

Topical delivery of keloid therapeutic drug, tranilast, by combined use of oleic acid and propylene glycol as a penetration enhancer: evaluation by skin microdialysis in rats.

Topical delivery of tranilast (N-(3,4-dimethoxycinnamoyl)anthranic acid), an inhibitor of collagen synthesis and a therapeutic drug for keloid and hypertrophic scar, was examined, in rats, with oleic acid alone or a combination of oleic acid and propylene glycol as penetration enhancer. Evaluation was by measurement of the concentration of tranilast in plasma and in the dialysate from skin microdialysis. When tranilast at a dose of 1.5 mg was applied topically as an ethanol solution containing 5% polyvinylpyrrolidone on a dorsal skin surface (2.25 cm2), the maximum concentration of tranilast in skin dialysate was approximately 2 microM. When 10 or 20% oleic acid was added to the same ethanol solution the maximum concentration of tranilast in the dialysate increased to 10-20 microM, and this value was further increased to 60 microM by the addition of a combination of oleic acid (10 or 20%) and propylene glycol (10%) to the solution. With the combination of oleic acid and propylene glycol the area under the plot of the concentration of tranilast in skin dialysate against time between 0 and 4 h (AUC0-4) was more than 400-fold that after intravenous administration. The transdermal bioavailability of tranilast as assessed by the AUC0-4 of tranilast in plasma, was 0.2% of the dose applied in the ethanol solution, 3-5% of that applied in the ethanol solution containing oleic acid, and 14-16% of that applied in the ethanol solution containing both oleic acid and propylene glycol. These results suggest that the topical delivery of tranilast with an absorption enhancer such as a mixture of oleic acid and propylene glycol might be a more effective medication than oral administration of tranilast for the treatment of keloid and hypertrophic scar.

Animals↗
PubMed2002

Abnormal pulmonary vascular tone in canine oleic acid lung injury.

OBJECTIVE: To characterize the endothelium-dependent and endothelium-independent components of abnormal pulmonary vascular tone in canine oleic acid lung injury. DESIGN: Prospective, interventional study. SETTING: University laboratory. SUBJECTS: Twenty anesthetized mongrel dogs. INTERVENTIONS: Right heart catheterization was performed to measure pulmonary vascular resistance before and after induction of oleic acid lung injury in ten anesthetized and ventilated dogs. Pulmonary and internal mammary artery rings were sampled in these ten dogs with oleic acid injury and in ten anesthetized healthy control dogs. We also studied the responses to acetylcholine, to phenylephrine, and to hypoxia of the intact or endothelium-denuded rings mounted in organ baths. MEASUREMENTS AND MAIN RESULTS: Oleic acid lung injury was associated with an increase in pulmonary vascular resistance from 118 +/- 11 to 245 +/- 47 dyne.sec.cm-5.m-2 and a decrease in the Pao2/Fio2 ratio from 451 +/- 42 to 139 +/- 26 mm Hg (mean +/- se, p <.05 and p <.01, respectively). Acetylcholine-induced relaxation was decreased in the oleic acid pulmonary artery rings compared with the controls (85 +/- 3% vs. 99 +/- 6% of precontraction level, p <.05). Phenylephrine-induced contraction was decreased in denuded oleic acid pulmonary artery rings compared with the controls (81 +/- 8% vs. 102 +/- 10% of contraction to KCl 120 mM, p <.05). In vitro hypoxia induced a small endothelium-dependent contraction followed by an endothelium-independent relaxation. These responses were not different in oleic acid lung artery rings and in controls, except for a decrease in hypoxic contraction in the oleic acid pulmonary artery rings. In vitro hypoxic pulmonary vasoconstriction and relaxation were, respectively, directly (r =.48) and inversely (r = -.67) correlated with oleic acid-induced increase in pulmonary vascular resistance. There was no correlation between in vitro internal mammary artery reactivity and oleic acid-induced increase in pulmonary vascular resistance. CONCLUSIONS: Oleic acid-induced lung injury slightly impairs pulmonary arterial endothelium-dependent relaxation and endothelium-independent contraction. In vitro hypoxic pulmonary vasoreactivity is related to in vivo oleic acid-induced increase in pulmonary vascular resistance.

Animals↗
PubMed1994

Oleic acid inhibition of Na+/D-glucose transport in isolated renal brush-border membranes: role of lipid physical parameters and trans Na(+)-inhibition.

UNLABELLED: Inhibition of Na+/D-glucose transport by oleic acid was investigated in renal brush-border membrane vesicles (BBMV). Lipid physical parameters were determined by spectrofluorometry. cis-Unsaturated C16-C22 long-chain fatty acids (LCFA) as oleic acid reduced nonzero limiting anisotropy r infinity with DPH and 12-AS as probes and decreased rotational correlation time phi of 12-AS. At 8 s and 15 s Na+/D-glucose transport was competitively inhibited. A positive correlation existed between decrease in r infinity (acyl chain order) or decrease in rotational correlation time phi (= increase in 'fluidity') and inhibition of Na+/D-glucose transport. Except elaidic acid trans unsaturated and saturated LCFA had no effect on fluorescence anisotropy and Na+/D-glucose transport. Per cent transport inhibition was unaffected by 0 voltage clamping and by FCCP. Ki for trans Na(+)-inhibition of D-glucose transport was 29 mmol/l. Na(+)-transport was stimulated by oleic acid, exceeding the Ki value for trans Na+ inhibition. CONCLUSION: oleic acid inhibits Na+/D-glucose transport by a decrease in lipid acyl chain order and an increase in 'fluidity', by trans Na(+)-inhibition and presumably by a third unknown mechanism.

Animals↗
PubMed2004

Treatment of skin papillomas with topical alpha-lactalbumin-oleic acid.

BACKGROUND: We studied the effect on skin papillomas of topical application of a complex of alpha-lactalbumin and oleic acid (often referred to as human alpha-lactalbumin made lethal to tumor cells [HAMLET]) to establish proof of the principle that alpha-lactalbumin-oleic acid kills transformed cells but not healthy, differentiated cells. METHODS: Forty patients with cutaneous papillomas that were resistant to conventional treatment were enrolled in a randomized, placebo-controlled, double-blind study, in which alpha-lactalbumin-oleic acid or saline placebo was applied daily for three weeks and the change in the volume of each lesion was recorded. After this first phase of the study, 34 patients participated in the second phase, an open-label trial of a three-week course of alpha-lactalbumin-oleic acid. Approximately two years after the end of the open-label phase of the study, 38 of the original 40 patients were examined, and long-term follow-up data were obtained. RESULTS: In the first phase of the study, the lesion volume was reduced by 75 percent or more in all 20 patients in the alpha-lactalbumin-oleic acid group, and in 88 of 92 papillomas; in the placebo group, a similar effect was evident in only 3 of 20 patients (15 of 74 papillomas) (P<0.001). After the patients in the initial placebo group had been treated with alpha-lactalbumin-oleic acid in the second phase of the study, a median reduction of 82 percent in lesion volume was observed. At follow-up two years after the end of the second phase, all lesions had completely resolved in 83 percent of the patients treated with alpha-lactalbumin-oleic acid, and the time to resolution was shorter in the group originally assigned to receive alpha-lactalbumin-oleic acid than among patients originally in the placebo group (2.4 vs. 9.9 months; P<0.01). No adverse reactions were reported, and there was no difference in the outcomes of treatment between immunocompetent and immunosuppressed patients. CONCLUSIONS: Treatment with topical alpha-lactalbumin-oleic acid has a beneficial and lasting effect on skin papillomas.

Administration, Cutaneous↗
PubMed2004

Pharmacologic enhancement of rat skin flap survival with topical oleic acid.

This study was instituted to investigate in a rat model the effect of topical coadministration of the penetration enhancer oleic acid (10% by volume) and RIMSO-50 (medical grade dimethyl sulfoxide, 50% by volume) on rat skin flap survival. A rectangular abdominal skin flap (2.5 x 3 cm) was surgically elevated over the left abdomen in 40 nude rats. The vein of the flap's neurovascular pedicle was occluded by placement of a microvascular clip, and the flap was resutured with 4-0 Prolene to its adjacent skin. At the end of 8 hours, the distal edge of the flap was reincised to gain access to the clips and the clips were removed. After resuturing of the flap's distal edge to its adjacent skin, the 40 flaps were randomly divided into four groups. Group 1 (control) flaps were treated with 5 g of saline, group 2 (dimethyl sulfoxide) flaps were treated with 2.7 g of dimethyl sulfoxide (50% by volume), group 3 flaps (oleic acid) were topically treated with 0.45 g of oleic acid (10% by volume), and group 4 (dimethyl sulfoxide plus oleic acid) flaps were treated with a mixture of 0.45 g of oleic acid (10% by volume) and 2.7 g of dimethyl sulfoxide (50% by volume) diluted in saline. Each flap was topically treated with 5 ml of drug-soaked gauze for 1 hour immediately after clip removal to attenuate reperfusion injury. Thereafter, drug was applied topically once daily for 4 more days. Digital photographs of each flap were then taken on day 6 and the flaps were then harvested. The percentage of skin survival in each flap was determined by computerized morphometry and planimetry. The mean surviving area of group 3 (oleic acid-treated flaps) was 23.60 +/- 4.19 percent and was statistically higher than that in group 1 (control, saline-treated flaps) at 7.20 +/- 2.56 percent. The mean surviving area of group 2 (dimethyl sulfoxide-treated flaps) at 18.00 +/- 5.23 percent and group 4 (oleic acid- and dimethyl sulfoxide-treated flaps) at 9.90 +/- 3.44 percent did not achieve statistically higher mean surviving areas than controls. A topical solution of oleic acid (10% by volume) caused a statistically significant increase in the survival of rat abdominal skin flaps relative to controls. Dimethyl sulfoxide and the two experimental drugs together did not increase the percentage of flap survival when given as a single 5-ml dose released from a surgical sponge at reperfusion for 1 hour and then daily for a total of 5 days. The reasons for the lack of response are unknown but may have included the technical difficulty of delivering an adequate dose of dimethyl sulfoxide topically and immiscibility between dimethyl sulfoxide and oleic acid. Further studies may be warranted.

Abdomen↗
PubMed2001

Signaling events mediating the additive effects of oleic acid and angiotensin II on vascular smooth muscle cell migration.

Obese hypertensive patients with cardiovascular risk factor clustering and increased risk for atherosclerotic disease have increased plasma nonesterified fatty acid levels, including oleic acid (OA), and a more active renin-angiotensin-aldosterone system. Vascular smooth muscle cell (VSMC) migration and proliferation participate in the development of atherosclerotic plaque. OA and angiotensin (Ang) II induce synergistic mitogenic responses in VSMCs through sequential signaling pathways dependent on the activation of protein kinase C (PKC), oxidants (reactive oxygen species, ROS), and extracellular signal-regulated kinase (ERK) activation. We tested the hypotheses that (1) OA and Ang II have additive or synergistic effects on VSMC migration and (2) PKC, ROS, and mitogen-activated protein kinase are critical signaling molecules. OA at 100 micromol/L increases VSMC migration 60+/-10% over control (P:<0.001). Ang II (10(-)(9) mol/L) increases VSMC migration by 62+/-13% and 73% over control, respectively (P:<0.01). Coincubation of cells with OA and Ang II produces a nearly additive increase in VSMC cell migration at 107+/-20% (P:<0.01). Increases in VSMC migration induced by OA alone and combined with Ang II were reduced by PKC inhibition and downregulation. VSMC migration in response to OA alone and with Ang II was also inhibited by N:-acetyl-cysteine, MEK inhibition, and ERK antisense. VSMC migration in response to OA alone or combined with Ang II is dependent on activation of PKC, ROS, and ERK activation, further raising the possibility that increased plasma nonesterified fatty acids and an activated renin-angiotensin-aldosterone system in subjects with the risk factor cluster contribute to accelerated atherosclerosis through a PKC, ROS, and ERK-dependent signaling pathway.

Acetylcysteine↗
PubMed2005

Dilution rate and pH effects on the conversion of oleic acid to trans C18:1 positional isomers in continuous culture.

In a previous in vitro study, mixed ruminal microorganisms converted oleic acid to a variety of trans monenes when grown in batch cultures under constant environmental conditions. To determine whether a similar conversion occurs under environmental conditions more typical of the rumen, conversion of 13C-labeled oleic acid to biohydrogenation intermediates was determined in ruminal microorganisms grown in continuous culture at two pH (5.5 and 6.5) and liquid dilution rates (0.05 and 0.10/h) arranged factorially. After each morning feeding of the dual-flow continuous cultures, 250 mg of oleic acid in 5 mL of ethanol were injected into each culture. On d 10, 250 mg of oleic-1-(13C) replaced the unlabelled oleic acid in ethanol. Trans fatty acids were isolated from culture samples by solid phase extraction, and 13C enrichment and identity of double bond position was determined by gas chromatography-mass spectroscopy. At pH 6.5 and 0.10/h dilution rate, 13C enrichment was detected in all trans-C18:1 isomers having double bond positions from C6 through C16 in the acyl chain. However, when pH or dilution rate in fermentors was lowered, no 13C enrichment was detected in any trans isomer with a double bond position beyond C10. Enrichment in stearic acid increased by reducing culture pH from 6.5 to 5.5, but decreased when dilution rate dropped from 0.10 to 0.05/h. The stearic acid carbons that originated from oleic acid biohydrogenation increased from 30 to 72% when pH dropped from 6.5 to 5.5. The 13C enrichment of trans-10 was reduced under low pH and dilution rate conditions. The results of this study confirm that ruminal microorganisms are capable of converting oleic acid to a wide variety of trans-C18:1 positional isomers when ruminal conditions are favorable (such as the pH 6.5 and 0.10/h dilution rate treatment). However, at low pH and dilution rate, the conversion of oleic acid to trans-C18:1 still occurs, but positional isomers produced are restricted to double bond positions from C6 to C10. Low pH conditions also increased the conversion of oleic acid to stearic acid.

Animals↗
PubMed1994

Secretion of oleic acid in milk fat in response to abomasal infusions of canola or high oleic sunflower fatty acids.

The feasibility of dietary strategies to increase oleic acid content of milk fat is unclear. Four Holstein cows were infused abomasally with free long-chain fatty acids from canola (62.5% C18:1) or high oleic sunflowers (86% C18:1). Each fatty acid mixture was infused for 3 d at 0, 133, 267, 400, 267, 133, and 0 g/d for a total of 21 d; cows then were changed to the opposite fatty acid mixture, and the infusion sequence was repeated. The DMI and percentages of casein and whey N in milk were decreased by infusion of fatty acids, but milk yield and percentages of fat and NPN in milk were increased. Contents of short- and medium-chain fatty acids and C16:0 in milk fat decreased, and contents of C18:1, C18:2, and C18:3 increased, as fatty acid infusion increased. Contents of C16:0 and C18:0 in plasma triglyceride were decreased, and content of C18:1 was increased, by increasing infusion of fatty acids. All changes reversed when the amount of fatty acid infused was decreased. Within the range of amounts of fatty acids infused, the relationship between yield of C18:1 in milk fat and the amount of C18:1 infused into the abomasum was linear, and transfer efficiency was 54.1%. Increased concentration and yield of C18:1 in milk were attributable mostly to the increased exogenous supply of C18:1.

Abomasum↗
PubMed1981

Effect of sodium nitroprusside on cardiovascular function and pulmonary shunt in canine oleic acid pulmonary edema.

The authors investigated the acute effects of nitroprusside on intrapulmonary shunt (Qs/Qt), cardiac output, and left ventricular function in dogs with normal lungs, and again after they developed oleic acid pulmonary edema. Before oleic acid, nitroprusside reduced pulmonary capillary wedge pressure (PCWP) and stroke volume, and there were no changes in Qs/Qt. Ninety minutes after oleic acid, PCWP, Qs/Qt, and systemic vascular resistance increased and stroke volume decreased. Then nitroprusside increased cardiac output by 35 per cent and increased Qs/Qt from 12 to 18 per cent. After oleic acid, stroke volume increased on nitroprusside from 18 to 23 ml (P less than 0.05) despite reduced preload, as PCWP decreased from 10.4 to 4.4 torr on nitroprusside (P less than 0.05). Increased stroke volume may be explained by the reduction in resistive afterload, as nitroprusside reduced systemic vascular resistance from 60 to 34 torr . l-1 . min. To the extent that canine oleic acid pulmonary edema represents low pressure edema in patients, nitroprusside is a potential treatment to reduce PCWP, pulmonary microvascular pressure, and pulmonary edema while maintaining cardiac output.

Animals↗
PubMed2006

Differential biohydrogenation and isomerization of [U-(13)C]oleic and [1-(13)C]oleic acids by mixed ruminal microbes.

The additional mass associated with 13C in metabolic tracers may interfere with their metabolism. The comparative isomerization and biohydrogenation of oleic, [1-(13)C]oleic, and [U-13C]oleic acids by mixed ruminal microbes was used to evaluate this effect. The percent of stearic, cis-14 and -15, and trans-9 to -16 18:1 originating from oleic acid was decreased for [U-(13)C]oleic acid compared with [1-(13)C]oleic acid. Conversely, microbial utilization of [U-(13)C]oleic acid resulted in more of the 13C label in cis-9 18:1 compared with [1-(13)C]oleic acid (53.7 vs. 40.1%). The isomerization and biohydrogenation of oleic acid by ruminal microbes is affected by the mass of the labeled tracer.

Analysis of Variance↗
PubMed1993

Bronchial vascular occlusion does not attenuate or accentuate oleic acid lung injury in anesthetized sheep.

To determine if bronchial blood flow affects the consequences of acute pulmonary vascular injury, we studied oleic acid lung injury in 12 anesthetized sheep. In six sheep (group 1), we injected 2 ml of ethanol directly into the bronchoesophageal artery to decrease bronchial blood flow. In the control sheep (group 2), we injected 2 ml of normal saline. One hour later, oleic acid (0.1 ml/kg) was injected into the right ventricle in both groups. We measured hemodynamics and lung mechanics at baseline, 1 h after injection into the bronchoesophageal artery but just before the injection of oleic acid, and 3 h after injection of oleic acid. We measured bronchial blood flow at baseline and 3 h after injection of oleic acid and extravascular lung water at 3 h after injection of oleic acid. One hour after injection of ethanol or saline into the bronchoesophageal artery, hemodynamics and lung mechanics did not change. Three hours after injection of oleic acid, systemic arterial pressure decreased, pulmonary arterial pressure increased, cardiac output decreased, dynamic compliance decreased, pulmonary resistance increased, arterial oxygen tension decreased, and extravascular lung water was greater than normal. There were no differences in these measurements between the two groups. However, bronchial blood flow decreased only in group 1. We conclude that decreasing bronchial blood flow does not attenuate or accentuate the consequences of oleic acid lung injury.

Animals↗
PubMed1979

Effect of oleic acid on insulin secretion by the isolated perfused rat pancreas.

The isolated perfused rat pancreas was utilized to investigate the effect of oleic acid on insulin secretion. In the absence of glucose, a continuous infusion of oleic acid (1500 micromol/l) induced a biphasic insulin release. This effect was reduced at low extracellular calcium concentration. In the presence of oleic acid 1500 micromol/l, the insulin response to 10 mmol/l arginine occurred earlier, the total amount of insulin released in response to the amino acid being unchanged. Such an effect was not obtained when oleic acid in the medium was 750 micromol/l, but it was observed in the presence of oleic acid 1500 micromol/l when the concentration of albumin in the perfusate was increased from 2 g/100 ml to 4 g/100 ml. The insulin response to a continuous infusion of glucose (4.4 mmol/l and 16.7 mmol/l) was potentiated by the presence of oleic acid 1500 micromol/l in the perfusate. No modification of the biphasic pattern of insulin response to glucose 16.7 mmol/l was observed. These results demonstrate that high concentrations of oleic acid stimulate insulin release from the isolated perfused rat pancreas and modulate the insulin response to arginine or glucose.

Animals↗
PubMed1975

[Oxidation of erucic acid and erucyl-CoA by isolated rat heart mitochondria: comparison to oleic acid].

The oxidation of [14 14-C] or [1 14-C] erucic acid by isolated mitochondria from Rat heart has been studied and compared with that of [10 14-C] oleic acid in varying conditions of incubation. Erucic acid is converted to CO2 and acid-soluble compounds much more slowly than oleic acid. The acid-soluble compounds which have been identified are acylcarnitines, ketone bodies and intermediates from the Krebs cycle; they are found in similar proportions for both substrates. Moreover, the oxidation rate of erucyl-CoA is comparable, if not equal, to that of oleyl-CoA in the same conditions. These results are discussed here. They lead to the conclusion that erucic acid is oxidized by isolated Rat heart mitochondria through the beta oxidation pathway, and that its oxidation is limited owing to its slow activation rate.

Animals↗
PubMed1996

Comparison of the effects of diets enriched in lauric, palmitic, or oleic acids on serum lipids and lipoproteins in healthy women and men.

The degree to which different saturated fatty acids exert their cholesterol-raising effects is still unknown. Therefore, we studied the effect on serum lipids and lipoproteins of diets rich in lauric, palmitic, or oleic acids. Eighteen women and 14 men consumed in random order three experimental diets, each for 6 wk. The diets consisted of solid foods and contained 40% of energy as fat, of which 28% was supplied by the experimental fats. The fat high in lauric acid was a mixture of palm kernel oil (75%) and a high-oleic acid sunflower oil (25%); the fat high in palmitic acid consisted of dairy fat (55%), palmstearin (36%), and sunflower oil (9%); and the fat high in oleic acid consisted of dairy fat (37%) and sunflower oil (63%). The calculated nutrient composition was the same in each diet except for approximately equal to 8.5% of energy, which was provided by lauric, palmitic, or oleic acids. With the lauric acid diet the subjects' serum total cholesterol concentration increased by 0.22 mmol/L (P = 0.0121; 95% CI: 0.02, 0.41 mmol/L) as compared with the palmitic acid diet and by 0.48 mmol/L (P < 0.0001; 95% CI: 0.29, 0.67 mmol/L) compared with the oleic acid diet. Total cholesterol concentrations with the palmitic acid diet were 0.26 mmol/L (P = 0.0012; 95% CI: 0.07, 0.46 mmol/L) higher than with the oleic acid diet. High-density-lipoprotein (HDL)-cholesterol concentrations increased by 0.12 mmol/L (P = 0.006; 95% CI: 0.04, 0.20 mmol/L) with the lauric acid compared with the palmitic acid diet and by 0.14 mmol/L (P < 0.001; 95% CI: 0.07, 0.22 mmol/L) compared with the oleic acid diet. HDL-cholesterol concentrations with the palmitic acid and the oleic acid diet were the same. No effects were seen in serum triacylglycerol and lipoprotein(a) concentrations. We conclude that both lauric and palmitic acids are hypercholesterolemic compared with oleic acid. Lauric acid raises total cholesterol concentrations more than palmitic acid, which is partly due to a stronger rise in HDL cholesterol.

Adult↗
PubMed1991

CCK and PYY do not participate in the delayed inhibition of pancreatic secretion, after stimulation by duodenal oleic acid infusion.

The role played by CCK in the stimulation of pancreatic secretion by duodenal infusion of oleic acid in conscious rats was studied using a potent and specific CCK receptor antagonist. CR-1409 did not alter basal secretion, which does not require CCK. The three doses of CR-1409 that were used (2, 4 and 8 mg/kg/h) suppressed the protein response to duodenal infusion of oleic acid and significantly enhanced the delayed inhibition normally observed in control rats (-81%, -87% and -88% vs. -51% of basal in controls). CR-1409 dose-dependently reduced the volume of pancreatic secretion after duodenal infusion of oleic acid (0.40 +/- 0.02, 0.36 +/- 0.02, 0.34 +/- 0.03 vs. 0.48 +/- 0.04 ml/30 min for 2, 4, 8 mg/kg/h and controls, respectively) and revealed a delayed inhibition of volume and a slight reduction of bicarbonate secretion. CCK appears to be directly responsible for the protein and also water response to duodenal infusion of oleic acid, and to be indirectly involved in bicarbonate stimulation. PYY antiserum significantly augmented protein output after duodenal infusion of oleic acid (10.75 +/- 1.40, 14.10 +/- 1.60 vs. 8.60 +/- 1.20 mg/30 min, 1 microliter, 2 microliters and controls), but failed to modify the delayed inhibition: PYY modulates the response to duodenal infusion of oleic acid and is not involved in the delayed inhibition, which was shown to be also present for volume, but which is normally masked by the action of CCK.

Animals↗