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Biomedical subjects

S Viau

Publications and source records attributed to S Viau.

At least 19 recordsLinked to original sources
PubMed2006

[Improvement of dry eye symptoms with polyunsaturated fatty acids].

INTRODUCTION: Polyunsaturated fatty acids (PUFAs) are involved in inflammatory pathways via prostaglandins. Conjunctival inflammation is a hallmark of all dry eye syndromes. We investigated the role of dietary n-6 and n-3 fatty acids in patients suffering from ocular dryness. PATIENTS AND METHODS: Seventy-one patients presenting with mild to moderate dry eye syndromes were randomly assigned to Nutrilarm or placebo capsules, twice a day for 6 months. The Schirmer test, BUT, fluorescein staining, and lissamin green stainings were performed at inclusion and after 1, 3, and 6 months. Furthermore, a questionnaire related to the dry eye symptoms and global discomfort was provided at every visit. RESULTS: The Schirmer test, BUT, fluorescein staining, and lissamin green stainings were improved with treatment when compared to placebo but the difference was not statistically significant. The efficacy evaluated by the patients and the investigator were nearly significant (p=0.052 and p=0.054, respectively). For some signs, such as reflex tearing and conjunctival hyperemia, the improvement reached the threshold of significance (p=0.047 and p=0.045, respectively). The same results were found with skin quality and emotional condition, which were improved (61% with treatment versus 36% with placebo). CONCLUSION: This double-masked pilot study shows that PUFAs seem to be an interesting tool to alleviate the symptoms related to dry eye syndrome. These results should be confirmed using a larger study population.

Double-Blind Method↗
PubMed1998

Effects of phosphoramidon, BQ 788, and BQ 123 on coronary and cardiac dysfunctions of the failing hamster heart.

Coronary dysfunctions identified in the presence of chronic heart failure are an important pathophysiologic abnormality that influences the prognosis of the disease. Because the endothelin pathway plays a significant role in the increased peripheral vascular tone associated with heart failure, we hypothesized that the endothelin pathway may be involved in the abnormal coronary vasomotion associated with this pathologic condition. Experiments were carried out in failing hearts (UM-X7.1 cardiomyopathic hamsters, aged 225-250 days) and normal hearts (Syrian LVG hamsters, also aged 225-250 days). Isolated hearts were perfused at constant flow and exposed to the blocker of the generation of endothelin-1 (ET-1), phosphoramidon (10 microM infusion), as well as to the selective ET(A)-receptor antagonist BQ 123 (10 microM infusion) and to a selective ET(B)-receptor antagonist BQ 788 (1 microM infusion). Coronary and cardiac effects of exogenous ET-1 (0.01-100 pmol) were also studied. Phosphoramidon, BQ 788, and BQ 123 did not altered coronary perfusion pressure either in normal or in failing hearts, whereas cardiac contractility was significantly impaired in the presence of phosphoramidon and BQ 123. Coronary sensitivity to exogenous ET-1 did not demonstrate a significant difference between normal and failing hearts [median effective concentration (EC50), 7 pmol in failing hearts vs. 12 pmol in normal hearts; p = NS]. In the presence of exogenous ET-1, cardiac contractility was significantly increased in both groups. In normal hearts, the exogenous ET-1-induced increase in coronary perfusion pressure was completely antagonized by BQ 123, whereas combined administration of BQ 788 and BQ 123 was necessary to induce complete inhibition in failing hearts. The positive inotropic effect elicited by exogenous ET-1 (EC50) was completely abolished in the presence of BQ 123, whereas BQ 788 had no significant effect. Results indicate that the endothelin pathway does not play a significant role in the altered coronary vasomotion observed in this model of chronic heart failure. On the contrary, the endothelin pathway appears to participate in the maintenance of myocardial contractility. According to these observations, administration of an inhibitor of ET-1 synthesis, as well as the use of an ET(A)-receptor antagonist, may be contraindicated in the presence of poor left ventricular function because the endothelin pathway contributes significantly to the maintenance of cardiac contractility.

Animals↗
PubMed1997

Myocardial reactive hyperemia in experimental chronic heart failure: evidence for the role of K+ adenosine triphosphate-dependent channels and cyclooxygenase activity.

BACKGROUND: Several studies suggest that coronary perfusion is abnormal in heart failure. The fact that these deficits may results in an altered coronary reserve remains controversial. Therefore, coronary adaptability to short-duration ischemia and the resultant myocardial reactive hyperemia were investigated in a model of chronic heart failure. METHODS AND RESULTS: Experiments were performed in normal and failing hamster hearts (UM-X7.1, aged > 225 days). Heart rate, left ventricular developed pressure, and coronary flow were recorded continuously before and after each 30-second ischemia in isolated perfused heart preparations. Studies were conducted under control conditions and in the presence of four inhibitors of potential mediators of the reactive hyperemia response: the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (30 microM), the adenosine antagonist 8-(p-sulfophenyl)theophylline (50 microM), the K+ cyclic adenosine triphosphate-dependent channel antagonist glibenclamide (10 microM), and the cyclooxygenase inhibitor indomethacin (10 microM). Baseline hemodynamic parameters were all significantly impaired in failing hearts. Under control conditions, failing hearts were able to respond adequately to a 30-second ischemia: repayment-to-debt ratio averaged 1.02 +/- 0.09 as compared with 1.10 +/- 0.09 in normal hearts (P = NS). All inhibitors significantly reduced basal coronary perfusion except for indomethacin. Of the four inhibitors of potential mediators of the myocardial reactive hyperemic response, only glibenclamide and indomethacin impaired the repayment-to-debt ratio. In their presence, repayment-to-debt ratio was reduced by 40% of the baseline response (P < .01) without significant difference between normal and failing hearts. On the contrary, NG-nitro-L-arginine methyl ester and 8-(p-sulfophenyl)theophylline did not alter the repayment-to-debt ratio. CONCLUSIONS: These observations demonstrate the capacity of the failing heart to tolerate short-duration ischemia despite the presence of significant alterations in its basal coronary perfusion. In addition, results suggest that activation of K+ adenosine triphosphate-dependent channels and the presence of cyclooxygenase by-products are important determinants of coronary adaptation to short-duration ischemia in this model of chronic heart failure.

Animals↗
PubMed1994

Cloning, sequencing, and expression in Escherichia coli of the D-hydantoinase gene from Pseudomonas putida and distribution of homologous genes in other microorganisms.

Pseudomonas putida DSM 84 produces N-carbamyl-D-amino acids from the corresponding D-5-monosubstituted hydantoins. The gene encoding this D-hydantoinase enzyme was cloned and expressed in Escherichia coli. The nucleotide sequence of the 1.8-kb insert of subclone pGES19 was determined. One open reading frame of 1,104 bp was found and was predicted to encode a polypeptide with a molecular size of 40.5 kDa. Local regions of identity between the predicted amino acid sequence and that of other known amidohydrolases (two other D-hydantoinases, allantionase and dihydroorotase) were found. The D-hydantoinase gene was used as a probe to screen DNA isolated from diverse organisms. Within Pseudomonas strains of rRNA group I, the probe was specific. The probe did not detect D-hydantoinase genes in pseudomonads not in rRNA group I, other bacteria, or plants known to express D-hydantoinase activity.

Amidohydrolases↗