Biomedical subjects

R Varin

Publications and source records attributed to R Varin.

7 recordsLinked to original sources

PubMed2005

[Transfusions of rhesus-incompatible platelet concentrates in Rouen University Hospital: procedures and consequences].

INTRODUCTION: Guidelines for distribution and use of blood products have been established for both blood transfusion institution and hospitals, in particular for the use of Rh (D)-incompatible platelet concentrates. The aim of this study was to evaluate: 1) the rate of attribution for the Rh (D)-incompatible platelets concentrates, 2) the immunisation prophylaxis practices, 3) the immunological consequences using short and medium term follow-up of transfused patients. METHODS: Patients with Rh (D)-incompatible platelets concentrate administered during the year 2003 at Rouen University Hospital were retrospectively selected. Patients on transfusion were described. The relationship of various factors with the injection as well as the appearance of allo-immunization was statistically tested. RESULTS: During a year, 280 Rh (D)-incompatible platelets concentrates were administered to 67 patients. Immunisation prophylaxis by injection of Ig anti-D was not systematically performed. Four immunizations in the Rhesus group system were identified: 2 against D antigen (Ag), 1 against E Ag and 1 against C Ag. Immunisations against D Ag occurred for two younger women considered as immunodeficient. Immunization prophylaxis was more frequent in poly-transfused patients. However no difference was observed for the other factors. CONCLUSION: Compatibility concerning Rhesus (D) is not always possible. The immunization against red cells persists, in particular against the antigens of the Rhesus group system and moreover for the immunodeficient patients. Recommendations for immunization prophylaxis by injection of specific anti-D immune-globulin (Ig) could be reconsidered.

Adolescent↗

PubMed2003

Adverse effect of polyvalent immunoglobulin in the treatment of Guillain-Barre syndrome.

BACKGROUND: Acute polyradiculoneuropathy or Guillain-Barre syndrome is a neurological disease which may present with severe forms which have a poor prognosis. The patient's management requires multidisciplinary specialised care. Morbidity has been reported to be significantly improved with initial therapy using high-dose intravenous immunoglobulin (IVIG). However, this therapy represent an immunological risk which has remained overlooked by clinicians in the majority of cases and is not clearly stated by the pharmaceutical companies. Therefore, the use of IVIG in the intensive care unit can cause some problems. CASE REPORT: A 32-year-old woman presented with clinical signs of Guillain-Barre syndrome. The patient received high-dose intravenous immunoglobulin (TEGELINE). Nine days after beginning therapy, she presented with severe immunological hemolytic anaemia; the IVIG was suspected as the cause. The blood cell count returned to normal approximately two months after the onset of the hemolytic syndrome. CONCLUSION: Despite the effectiveness of IVIG therapy in the management of various diseases, intensive care clinicians should be aware of possible major adverse effects which make a careful assessment of the patient necessary before treatment. It may also be important to consider the patient's ABO blood group before initiating IVIG treatment, particularly in patients bearing A and/or B blood group antigens.

ABO Blood-Group System↗

PubMed2000

Improvement of endothelial function by chronic angiotensin-converting enzyme inhibition in heart failure : role of nitric oxide, prostanoids, oxidant stress, and bradykinin.

BACKGROUND-Chronic heart failure (CHF) impairs the endothelium-dependent, flow-mediated dilation (FMD) of small arteries. However, whether chronic angiotensin-converting enzyme (ACE) inhibition affects the impairment of FMD in CHF is unknown. We investigated the effects of long-term ACE inhibition on the FMD of peripheral arteries in rats with CHF and the mechanism(s) involved. METHODS AND RESULTS-FMD was assessed in isolated, perfused gracilis muscle arteries from sham-operated, and untreated or ACE inhibitor-treated (perindopril 2 mg. kg(-1). day(-1) for 10 weeks) rats with CHF (coronary artery ligation). The role of nitric oxide (NO), prostaglandins, and free radicals was assessed by pretreating the vessels with the NO synthase inhibitor N(W)-nitro-L-arginine, the cyclooxygenase inhibitor diclofenac, or the free radical scavenger N-2-mercaptopropionyl-glycine (MPG). Endothelial NO synthase mRNA expression was determined by reverse transcriptase polymerase chain reaction. In animals with hemodynamic and echographic signs of CHF, FMD was converted into vasoconstriction, and this was prevented by ACE inhibition. FMD of arteries from sham-operated or ACE inhibitor-treated CHF rats was abolished by N(W)-nitro-L-arginine. In untreated CHF rats, FMD was increased by diclofenac and MPG. In contrast, in arteries from ACE inhibitor-treated rats, neither diclofenac nor MPG affected FMD. In parallel, ACE inhibition prevented the reduction of endothelial NO synthase mRNA by CHF. CONCLUSIONS-In CHF, ACE inhibition normalized NO-dependent dilatation and suppressed the production of vasoconstrictor prostanoid(s), resulting in improved FMD. The improvement of FMD might contribute to the beneficial effects of ACE inhibition during CHF.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1999

Exercise improves flow-mediated vasodilatation of skeletal muscle arteries in rats with chronic heart failure. Role of nitric oxide, prostanoids, and oxidant stress.

BACKGROUND: Flow-mediated dilatation (FMD) of the peripheral arteries may be impaired in chronic heart failure (CHF), and this could contribute to the increased peripheral resistance and exercise intolerance that occur with this disease. Physical exercise improves the FMD of large conduit arteries in CHF, but whether a similar impairment also occurs in smaller arteries is unknown. The mechanisms of the changes in FMD after CHF or exercise are also unknown. METHODS AND RESULTS: FMD was assessed in isolated, perfused, and preconstricted gracilis muscle arteries from sham-operated rats or CHF rats (coronary artery ligation) who were either sedentary or exercised (30-minute swimming period twice a day for 10 weeks, starting 7 days after ligation). In animals with hemodynamic and echographic signs of CHF, FMD was abolished and converted into vasoconstriction (percent change in diameter after 370 microL/min flow: sham, 42+/-5%; CHF, -4+/-3%; P<0.05). Exercise partially restored FMD (18+/-3%; P<0.05 versus CHF). In sham rats, FMD was abolished by the nitric oxide-synthase inhibitor Nomega-nitro-L-arginine (L-NA) but unaffected by the cyclooxygenase inhibitor diclofenac or the free radical scavenger N-(2-mercaptopropionyl)-glycine (MPG). In arteries from sedentary CHF rats, FMD was not modified by L-NA, but it was partially restored by diclofenac or MPG. In exercised CHF rats, FMD was abolished by L-NA and only moderately improved by diclofenac or MPG. Likewise, endothelial nitric oxide synthase mRNA expression (determined by reverse transcription polymerase chain reaction at the level of the gracilis muscle) was reduced by CHF, and this was prevented by exercise. CONCLUSIONS: CHF abolishes the FMD of small arteries by impairing the nitric oxide pathway, increasing oxidant stress, and releasing a prostanoid-contracting factor. Exercise partially restores FMD by increasing expression of endothelial nitric oxide synthase and preventing the production of vasoconstrictor prostanoids and free radicals. Such restoration of FMD might contribute to the increase in exercise capacity after physical exercise in CHF.

Animals↗

PubMed1997

[Endothelial dysfunction in cardial failure: potential mechanisms].

From the vascular point of view, cardiac failure is characterised by increased systemic resistances secondary to an increased concentration of a number of vasoconstrictor substances and also to decreased endothelium dependent vasodilatation. Endothelial dysfunction has been described both in man and in animal models, but its causes are not well understood. Such dysfunction could be due to a decrease in the production of nitric oxide, a decrease in its vasodilator effect due to an increased degradation or an increased vasoconstrictor tone. Recent data suggests an improvement or prevention of this endothelial dysfunction observed in cardiac failure by physical training and by chronic treatment with an angiotensin converting enzyme inhibitor. The improvement or preservation of endothelial function induced by exercise or ACE inhibitor could explain some of the benefits of these treatments in terms of tissue perfusion and haemodynamic conditions.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1981

A clinical study of quazepam in hospitalized patients with insomnia.

The efficacy of quazepam (Sch-16134) 15 mg capsules as a hypnotic has been compared with that of placebo in a 9-day study, using a parallel-group design. The physician's global evaluation numerically favoured quazepam 63% (nineteen of thirty) over placebo 50% (fifteen of thirty). Furthermore, it demonstrated greater improvement in Hypnotic Activity Index and Sleep Quality Index from baseline scores, and caused no adverse reactions.

Adolescent↗

PubMedDate not supplied

[Oxidative stress and endothelial dysfunction in heart failure].

Chronic heart failure is characterized by increased vascular systemic resistances secondary to activation of various vasoconstrictor systems and to decreased endothelium-dependent vasodilatation. Endothelial dysfunction, described both in animals and in humans, may be caused by an increased inactivation of nitric oxide (NO) by reactive oxygen species, leading to decreased NO bioavailability and impaired vasodilatation. Increased levels of free radicals in heart failure may result either from increased production or a decrease in the cellular antioxidant reserves. Free radicals are produced by three enzymatic systems: NADH/NADPH oxidase (after stimulation by angiotensin II or TNF-alpha), xanthine oxidase or endothelial NO-synthase (NOS) itself. However, oxidative stress alone cannot explain endothelial dysfunction. Other mechanisms involved in the regulation of the production of NO (e.g. decreased expression and/or activity of the NOS) and/or changes in production of vasoconstrictors may participate in this impaired endothelium-dependent vasodilatation in heart failure.

Animals↗