Biomedical subjects

Annie Beauséjour

Publications and source records attributed to Annie Beauséjour.

5 recordsLinked to original sources

PubMed2006

Characterization of blood components prepared from whole-blood donations after a 24-hour hold with the platelet-rich plasma method.

BACKGROUND: The preparation of platelet (PLT) concentrates (PCs) from PLT-rich plasma (PRP) requires that whole blood (WB) be processed within 8 hours of collection. Increasing WB storage time to 24 hours would be logistically attractive. This study compares the in vitro quality of blood components prepared from WB stored for 8 and 24 hours at room temperature before processing with the PRP method. STUDY DESIGN AND METHODS: WB units were collected from ABO-matched blood donors. To reduce individual variations, paired donations were drawn in parallel, pooled, and split back in the collection bag. One unit was held for 6 to 8 hours and the other for 22 to 24 hours at 20 to 24 degrees C. Prestorage leukoreduced components were prepared with the PRP as intermediate product and analyzed during storage. RESULTS: RBC units prepared after an 8- or 24-hour hold were comparable in terms of hemolysis, sodium, pH, and ATP levels. RBC 2,3- diphosphoglycerate (2,3-DPG) was significantly lower in RBCs prepared from 24-hour hold donations immediately after processing but not after 20 days of storage. Residual white blood cells were approximately fivefold higher (p < 0.05) in 24-hour RBC units. For PCs, measurements for glucose, ATP, lactate, pH, extent of shape change, hypotonic shock response, and CD62p activation were similar. No differences were observed in the von Willebrand factor, factor (F)V, FVIII, and fibrinogen content of fresh-frozen plasma. CONCLUSIONS: The decrease in FVIII and RBC 2,3-DPG can be acceptable as a compromise to improve blood component logistics, but leukoreduction efficiency must be improved before considering the adoption of an overnight storage of WB before PRP processing.

ABO Blood-Group System↗

PubMed2006

Establishment of an immunoglobulin A-deficient blood donor registry with a simple in-house screening enzyme-linked immunosorbent assay.

BACKGROUND: Transfusion of blood products to immunoglobulin A (IgA)-deficient patients who have developed IgA antibodies can result in serious adverse reactions. To prepare compatible blood components for these patients, blood centers usually maintain a list of IgA-deficient blood donors. An in-house enzyme-linked immunosorbent assay (ELISA) was used to identify new IgA-deficient blood donors. STUDY DESIGN AND METHODS: An in-house ELISA was used to screen blood samples. IgA-deficient samples, defined as an IgA level below 0.05 mg per dL, were sent to the American Red Cross for confirmatory testing. RESULTS: Seventy-three confirmed IgA-deficient blood donors were identified among 38,759 screened blood donor samples (frequency, 1:531). IgA antibodies were found in 39 of these 73 blood donors (53%), although only 9 donors had a history of adult IgA exposure (transfusion or pregnancy). CONCLUSIONS: With a simple in-house ELISA, 73 blood donors were identified as IgA-deficient. From this number, 34 donors, without detectable anti-IgA in their plasma, were added to our IgA-deficient blood donor panel to maximize the management of our inventory of IgA-deficient frozen blood components.

Antibodies, Anti-Idiotypic↗

PubMed2006

Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake.

Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin-angiotensin-aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low- and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na+) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 microm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 micromol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.

Aldosterone↗

PubMed2004

Increased Na+ intake during gestation in rats is associated with enhanced vascular reactivity and alterations of K+ and Ca2+ function.

Gestation is associated with decreased blood pressure and resistance to the effects of vasoconstrictor agents. A recent study showed that pregnant rats, on increased sodium intake, present physiological changes that resemble those observed in preeclampsia. We investigated the effects of sodium supplementation on reactivity and on potassium and Ca(2+) channel activity in blood vessels during gestation. Sodium supplements, 0.9% or 1.8% NaCl as drinking water, were given to nonpregnant and pregnant rats for 7 days (last week of gestation). Reactivity to phenylephrine (PE), KCl, arginine vasopressin (AVP), and tetraethylammonium (TEA) was measured in aortic rings under modulation of potassium and calcium channels. TEA, a nonselective K(+) channel inhibitor, induced concentration-dependent responses in aortic rings from nonpregnant but not in those from pregnant rats. The response to TEA was restored in rings from pregnant rats after preincubation with 10 mmol/l KCl. Sodium supplementation did not affect the response to TEA in the aortas of pregnant animals. After sodium supplementation, maximum responses to PE and AVP were decreased and increased in aortic rings from nonpregnant and pregnant rats, respectively. Cromakalim (an ATP-sensitive K(+) channel activator)-induced inhibition of the responses to the three vasoconstrictors was more striking in aorta from nonpregnant than pregnant rats on regular diet, whereas it produced similar inhibition in tissues from both groups of animals on 0.9% and 1.8% NaCl. NS-1619 (a Ca(2+)-sensitive K(+) activator) elicited heightened effects in the aortas of pregnant animals receiving 0.9% NaCl supplementation. Nifedipine (a Ca(2+) channel blocker) caused greater inhibition of the contractile responses in tissues from nonpregnant rats on regular diet, and its action was increased in pregnant rats on sodium-supplemented diets. These data demonstrate that augmented sodium intake during gestation in the rat is linked with the reversal of gestational-associated resistance to vasopressors and indicate that this is an experimental model showing some features of gestational hypertension.

Animals↗

PubMed2003

High-sodium intake prevents pregnancy-induced decrease of blood pressure in the rat.

Despite an increase of circulatory volume and of renin-angiotensin-aldosterone system (RAAS) activity, pregnancy is paradoxically accompanied by a decrease in blood pressure. We have reported that the decrease in blood pressure was maintained in pregnant rats despite overactivation of RAAS following reduction in sodium intake. The purpose of this study was to evaluate the impact of the opposite condition, e.g., decreased activation of RAAS during pregnancy in the rat. To do so, 0.9% or 1.8% NaCl in drinking water was given to nonpregnant and pregnant Sprague-Dawley rats for 7 days (last week of gestation). Increased sodium intakes (between 10- and 20-fold) produced reduction of plasma renin activity and aldosterone in both nonpregnant and pregnant rats. Systolic blood pressure was not affected in nonpregnant rats. However, in pregnant rats, 0.9% sodium supplement prevented the decreased blood pressure. Moreover, an increase of systolic blood pressure was obtained in pregnant rats receiving 1.8% NaCl. The 0.9% sodium supplement did not affect plasma and fetal parameters. However, 1.8% NaCl supplement has larger effects during gestation as shown by increased plasma sodium concentration, hematocrit level, negative water balance, proteinuria, and intrauterine growth restriction. With both sodium supplements, decreased AT1 mRNA levels in the kidney and in the placenta were observed. Our results showed that a high-sodium intake prevents the pregnancy-induced decrease of blood pressure in rats. Nonpregnant rats were able to maintain homeostasis but not the pregnant ones in response to sodium load. Furthermore, pregnant rats on a high-sodium intake (1.8% NaCl) showed some physiological responses that resemble manifestations observed in preeclampsia.

Animals↗