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Biomedical subjects

C Deby

Publications and source records attributed to C Deby.

At least 73 records · Page 4Linked to original sources
PubMed1989

Differences in tocopherol-lipid ratios in ARDS and non-ARDS patients.

Plasma tocopherol, plasma total lipid levels and tocopherol-lipid ratio were measured every 6 h during 48 h in 12 critically ill patients and compared with those of a control group. The patients were divided into two groups. Group I comprised 6 critically ill patients with ARDS and group II comprised 6 severely ill patients without ARDS. The means for all observations of plasma tocopherol, total lipid levels and tocopherol-lipid ratio in groups I and II were significantly depressed relative to a control group (p less than 0.0001). The difference in the average tocopherol-lipid ratio between the three groups (p less than 0.0001) and between the groups I and II was statistically significant (p less than 0.0001). Our results indicated: (1) a decrease of vitamin E concentrations in the critically ill patients, particularly in ARDS patients; (2) the importance of the relationship between plasma tocopherol and plasma lipids levels in evaluating the deficiency in vitamin E which was evident in ARDS patients.

Adult↗
PubMed1989

[Effect of cicletanine on prostacyclin generation in vivo].

The administration of arachidonic acid to live rabbits if followed by the generation of prostacyclin and/or thromboxane. Cicletanine increased the production of prostacyclin in a first group of rabbits and amplified the prostacyclin/thromboxane ratio in a second group of the thromboxane type. The most probable mechanism for this action is activation of prostacyclin synthase by cicletanine. This was confirmed in the in vivo model by a study of the platelet-vascular wall interaction: tranylcyprominE, a prostacyclin synthase inhibitor, increased the interaction. Under these experimental conditions, cicletanine inhibited the effect of tranylcypromine and completely restored the enzymatic activity of prostacyclin synthase.

Animals↗
PubMed1989

[Effects of treatment with cicletanine on kidney PGE2 and PGI1 in spontaneously hypertensive rats].

Cicletanine is a new antihypertensive agent known for being able to stimulate prostaglandin synthesis in vivo and in endothelial cell cultures. The drug was administered to spontaneously hypertensive rats (SHP-SP) whose hypertension was enhanced by a high sodium content diet. Cicletanine prolonged the animals' survival and reduced the severity of histological renal lesions. PGE2, PGI2 and thromboxane A2 assays performed in renal tissues showed a highly significant increase of PGE2 (a prostaglandin involved in the regulation of renin synthesis) in SHR-SP rats treated with oral cicletanine in daily doses of 30 mg/kg. A less significant increase of PGI2 was found in renal tissues, whereas only slight variations in thromboxane concentrations were observed. The favourable therapeutic effect obtained with cicletanine in the treatment of hypertension may be due, at least in part, to the stimulation of PGE2 and PGI2 production in renal tissue.

Animals↗
PubMed1988

Human myeloperoxidase activity is inhibited in vitro by quercetin. Comparison with three related compounds.

Quercetin is an effective inhibitor of human myeloperoxidase (MPO) activity, both with purified enzyme (IC50 = 3.5 microM) and in a system using stimulated human neutrophils. Quercetin is significantly more potent than three other related compounds (rutin, rutin sulfate and troxerutin) and than methimazole, a previously-known myeloperoxidase inhibitor. The inhibitory activity of quercetin is of the competitive type. Moreover, quercetin is directly able to scavenge hypochlorous acid (HOCl), a chlorinated species generated by the MPO/H2O2/Cl- system.

Chemical Phenomena↗
PubMed1988

Tocopherol mobilization during intensive exercise.

This work shows that the level of plasma tocopherol (vitamin E) which has free radical scavenging properties rises significantly during intensive exercise. It is proposed that mobilization of tocopherol could help to prevent lipoperoxidation phenomena occurring in exercising skeletal muscle. A hypothetical mechanism relating to a lipolysis effect is discussed to explain this mobilization.

Adult↗
PubMed1988

Modulation of prostacyclin synthetase by cicletanine and drugs which affect ion transport.

Cicletanine, a drug which affects membrane ion transport, induces a marked increase of the liberation of PGI2 as demonstrated by the increase of the stable metabolites in the plasma following intravenous administration of arachidonic acid. Furthermore, the inhibiting effect of tranylcypromine on prostacyclin synthetase is completely removed by this pharmacon. These observations are suggestive that this drug presents a scope for treatment of thrombotic disorders as well as hypertension.

Animals↗
PubMed1988

Modulation of in vivo generation of prostanoids by drugs affecting membrane ion transport.

An in vivo animal model was developed in the rabbit for the study of the mechanisms involved in the generation and release of prostanoids. Following heparinization and, if required, further sensitization of the animals by intravenous administration of haemolysed blood, injection of doses of arachidonic acid not exceeding 180 micrograms/kg induced a marked fall in arterial blood pressure on condition that the plasma anti-inflammatory protein levels were within the normal range. Cicletanine, certain diuretics (furosemide and bumetanide), as well as calcium-entry blockers such as verapamil and the association of insulin and potassium ions, all markedly decreased the AA50 value and were accompanied by a significant increase in the plasma levels of 6-oxo-PGF1 alpha, enhancing as such the ratio of 6-oxo-PGF1 alpha versus TXB2 in plasma. The infusion of insulin in association with potassium ions induced a similar but less sustained effect. Drugs which affect membrane ion transport were investigated in relation to an enhancing effect on the generation and release of prostanoids following the administration of arachidonic acid.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Enhancement of prostacyclin generation by cicletanine (an in vivo investigation).

The effect of cicletanine, an antihypertensive drug, was studied in two in vivo models. It was demonstrated that the drug markedly affected the response of intravenously administered arachidonic acid in the rabbit. In this model a marked increase of 6-oxo-PGF1 alpha was observed when challenged by the intravenous injection of 50 micrograms/kg b.w. of arachidonic acid. In the rat model used for the study of platelet-vessel wall interaction, it was demonstrated that the inhibition of prostacyclin synthetase could be offset by cicletanine. These results indicate that the drug modulates the generation of prostacyclin and as such is capable of affecting the peripheral resistances which determine the level of the blood pressure.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

[Increase of the prostacyclin/thromboxane A2 ratio in the plasma of rabbits treated with cicletanine, a new antihypertensive agent].

An animal model was developed, permitting the study of thromboxane A2 and prostacyclin neoformation, after arachidonic acid (AA) injection. Two types of physiopathological responses were observed, according to the rabbit strains. In the first type, prostacyclin neoformation was predominant, AA injection inducing only reversible hypotension. In the second type, thromboxane A2 neoformation was prevalent, AA injection inducing irreversible hypotension, marked myocardial troubles, shock, and death. In both types, injection of cicletanine (5 x 10(-5) mole/kg) significantly enhanced prostacyclin neoformation. After cicletanine, a new hypertensive drug, rabbits of the second type responded like those of the first type, without severe physiopathological responses to AA injections.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Ginkgo biloba extract inhibits oxygen species production generated by phorbol myristate acetate stimulated human leukocytes.

A Ginkgo biloba extract (Gbe) containing flavonoids, among other compounds, was tested for the release of activated oxygen species (O-2, H2O2, OH.) during the stimulation of human neutrophils (PMNs) by a soluble agonist. The extract slows down O2 consumption (respiratory burst) of stimulated cells by its inhibitory action on NADPH-oxidase, the enzyme responsible for the reduction of O2 to O-2. Consequently, superoxide anion (O-.2) and hydrogen peroxide (H2O2) production is significantly decreased when the PMNs stimulation is done in the presence of the extract at concentrations of 500, 250 and 125 micrograms/ml. Moreover, the hydroxyl radical generation (OH.) is very much decreased at concentrations as low as 15.6 micrograms Gbe/ml, which indicates that the extract also has free radical scavenging activity. Gbe is able at least to reduce very severely the activity of myeloperoxidase contained in neutrophils. This enzyme, secreted into the intra and extracellular medium, catalyzes the oxidation of chloride (Cl-) by H2O2 to yield strong oxidants (HOCl, chloramines) which are implicated in inflammatory processes.

Free Radicals↗
PubMed1987

Thromboxane and prostacyclin release in adult respiratory distress syndrome.

Plasma thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured in 84 patients at risk of developing adult respiratory distress syndrome (ARDS) (44 patients following multiple trauma, 29 patients following abdominal surgery and 11 patients with acute pancreatitis). Forty-nine of these 84 patients developed an ARDS. High (greater than 140 pg/ml plasma) TXB2 values were found in 52/84 patients. The median values of TXB2 were: 360 pg/ml in multiple injured, 250 pg/ml in abdominal surgery and 410 pg/ml in acute pancreatitis patients. The median TXB2 value was 575 pg/ml in patients developing ARDS and 140 pg/ml in those without this complication: this difference was statistically significant (p less than 0.05). The median values of 6-keto-PGF1 alpha were 55 pg/ml in multiple injured, 25 pg/ml in abdominal surgery and 120 pg/ml in acute pancreatitis patients. The median 6-keto-PGF1 alpha value was 122 pg/ml in ARDS patients and 25 pg/ml in non-ARDS patients (statistically significant: p less than 0.05). High TXB2 and 6-keto-PGF1 alpha values were particularly related to sepsis in abdominal surgery patients (p less than 0.05) and in multiple injured patients (p less than 0.01). No relation could be established between abnormal TXB2 or 6-keto-PGF1 alpha values and death. High TXB2 values often persisted for several days and were observed particularly at the time ARDS diagnostic criteria were fulfilled.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Antiradical properties of Ginkgo biloba extract].

The anti-radical properties of Ginkgo biloba extract have been determined on several in vitro models. The products is as effective as uric acid, an anti-radical agent known to entrap the hydroxyl and diphenylpicrylhydrazyl radicals. In addition, it inactivates the formation of radicals, such as adriamycyl, which escape uric acid activity. It also inhibits membrane lipid peroxidation and owes to its anti-radical activity exerts a stimulant effect on the biosynthesis of prostanoids.

Animals↗
PubMed1986

[Toxicity of oxygen, free radicals and defense mechanisms].

Oxygen is essential for the life of aerobic organisms as the terminal acceptor of electrons. Due to its high affinity for lone electrons it fosters radicular reactions and opposes recombinations of radicals after rupture of covalent linkages. Lipoperoxidation processes then occur, attacking the cellular membranes. These radicular reactions are at the origin of many pathological phenomena. A complex arsenal of endogenous protective agents is normally present in all cells to face up to the danger of lone electron structures in oxygenated media. Food and natural or synthetic pharmacological agents compensate for the deficiencies.

Aerobiosis↗
PubMed1986

Stimulation of cyclooxygenase by activated human neutrophils is enhanced by uric acid.

Activated human neutrophils supernatant enhances prostanoids production by bull seminal cyclooxygenase (455% of control). Superoxide anion and hydrogen peroxide are not involved in this stimulation, in these experimental conditions. Myeloperoxidase (by its hemic nature) and HPETEs (by their -OOH function) could trigger cyclooxygenase. In the presence of uric acid (10(-3) M), a potent hydroxyl radical scavenger, the cyclooxygenase stimulation by supernatant is increased until 709% of the control.

Animals↗
PubMed1986

Trypsin-like activity and thromboxane release in adult respiratory distress syndrome.

Plasmatic immunoreactive trypsin (IRT), thromboxane and trypsin-like enzymatic activity were measured in 117 patients at risk of developing adult respiratory distress syndrome (ARDS) (53 multiple injury, 30 abdominal surgery, 17 acute pancreatitis, 12 burnt and 5 disseminated intravascular coagulation patients). 69 of these patients developed ARDS. Immunoreactive trypsin and thromboxane were measured by radio-immuno-assay and trypsin-like enzymatic activity by spectrophotometry, using a specific chromogenic substrate. Mean IRT value was 675 ng/ml in ARDS and 265 ng/ml in non ARDS patients (p less than 0.05). Mean IRT value was 685 ng/ml in septic and 170 ng/ml in non septic patients (p less than 0.01). An abnormal trypsin-like enzymatic activity was measured in 26 ARDS patients. In 60 patients (37 ARDS and 23 non ARDS), thromboxane appeared in plasma simultaneously or about 24 hours after the beginning of IRT release. The importance of thromboxane release parallels the intensity of IRT. Originating from pancreas, trypsin can appear in plasma either by absorption from gastrointestinal tract or after pancreatic ischemia.

Clinical Enzyme Tests↗
PubMed1986

Consumption of pentane by hepatic microsomes and consequences on pentane measurement in exhaled gases.

Pentane measurement in exhaled gases was proposed as a safe method to evaluate the importance of lipoperoxidation in vivo, in man and in animals. However we have observed that pentane, which arises from lipoperoxide decomposition, is significantly consumed by cytochrome P-450-rich liver microsomes. This pentane consumption is completely inhibited after heating the microsomes at 100 degrees C, and is considerably reduced by metyrapone, a cytochrome P-450 inhibitor. Hepatic metabolism of pentane, particularly after cytochrome P-450 induction, constitutes a risk of error, when pentane exhalation is taken as an index of lipoperoxidation in vivo.

Animals↗