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Biomedical subjects

M Beaufils

Publications and source records attributed to M Beaufils.

At least 37 records · Page 2Linked to original sources
PubMed1994

Subpicogram determination of oxytocin by an enzyme immunoassay using acetylcholinesterase as label.

The pure tetrameric form of Acetylcholinesterase (EC-3.1.1.7) from the electric eel electrophorus electricus has been covalently coupled to oxytocin. This conjugate has been used as tracer in a heterologous competitive immunoassay. Microtiter plates coated with a mouse monoclonal anti-rabbit immunoglobulin antibody were used to separate bound and free moieties of the tracer. Acetylcholinesterase activity bound to the solid phase was measured by a colorimetric assay. The minimum detectable concentration was 0.075 pg/well (ie 1.5 pg/ml) and precision was less than 8% at concentration above 0.15 pg/well. An extraction step improved sensitivity up to 10 times with good recoveries. To assess the validity of this assay, basal levels of oxytocin were measured during the oestrous cycle of a cow.

Acetylcholinesterase↗
PubMed1993

[Pregnancy nephropathies].

Our understanding of the pathophysiology underlying the hypertensive diseases of pregnancy has clearly progressed during the past ten years. The key phenomenon is an early defect of placentation occurring at the end of the first trimester and associated with a more widespread endothelial disorder. This results in early activation of the coagulation cascade and imbalance between prostacyclin and thromboxanes. Hypertension and proteinuria only occur after several weeks or months of placental dysfunction. This explains why antihypertensive treatments are ineffective in improving the prognosis of such pregnancies. In contrast, early preventive treatments, such as antiplatelet therapy, seem to be very promising for these patients. In this respect, early prediction of the risk associated with pregnancy has become a key goal.

Adult↗
PubMed1993

[Hypertension and pregnancy: physiopathology, treatment, prevention].

Pathophysiologic understanding of the hypertensive diseases of pregnancy has largely progressed in the past 10 years. The key phenomenon is an early defect of placentation, occurring at the end of first trimester. It is associated with a more global endothelial disorder. This results in early activation of coagulation, and an imbalance between prostacyclin and thromboxanes. Hypertension and proteinuria only occur after several weeks or months of placental dysfunction. This explains why antihypertensive treatments are ineffective in improving the prognosis of such pregnancies. On the contrary, early preventive treatments, such as antiplatelet therapy, seem very promising for those patients.

Female↗
PubMed1993

Preserving the autoregulation of renal hemodynamics.

Renal hemodynamics in essential hypertensives is characterized by an increase in renal vascular resistance (RVR) and a decrease in renal plasma flow (RPF), while glomerular filtration rate (GFR) is either normal or slightly decreased. Filtration fraction (FF) is increased, indicating that vasoconstriction predominantly affects postglomerular arteries. This increase in FF, called hyperfiltration, can be regarded as a successful maintenance of a normal glomerular filtration but can be deleterious for long-term renal function by favoring the development of glomerulosclerosis. Administration of some beta-blockers (especially propranolol) to hypertensive patients still reduces RPF and GFR, and increases FF. Conversely, in short-term studies, tertatolol has been shown to reduce RVR and increase RPF, without altering FF in hypertensive patients. These effects correspond to a normalization of the renal hemodynamic profile. Their practical interest is however strongly dependent on their persistence in long-term treatment. The beneficial effects of tertatolol were confirmed in 3 long-term studies, lasting for one year. These three studies yielded remarkably similar results: there was a modest overall decrease in serum creatinine, and a more pronounced drop in patients whose pretreatment renal function was altered. These data suggest that tertatolol may preserve the long-term autoregulation of renal hemodynamics. The possibility is raised that in patients with minimal renal dysfunction, tertatolol may also slow down the progression of renal failure.

Adrenergic beta-Antagonists↗
PubMed1993

[Influence of the number of corpora lutea on the release of luteal oxytocin, the transfer of alveolar milk to the cistern and milk production in the ewe].

This experiment was conducted in 59 Lacaune breed ewes in order to compare milk production and milk distribution between alveolar and cisternal storage after superovulation. After a corpora lutea (CL)-free control period, the ewes were superovulated by different treatments (experimental period) and 5 classes were differentiated according to the number of corpora lutea observed (0, 1, 2, 3 to 6 and > 6 CL respectively (group A (n = 20), B (n = 7), C (n = 14), D (n = 7), E (n = 11)). Our results showed a positive correlation between the number of corpora lutea and the oxytocin and progesterone levels in plasma, total milk production and cisternal volume, and a negative correlation with alveolar volume. The milk production at the evening milking for groups A and E (388.6 and 384.8 ml respectively during the control period) respectively reached 321.7 ml (-17.2%) and 413.4 ml (+7.4%) during the experimental period; ie, a 24.6% difference between these 2 extreme groups. These results could likely be explained by oxytocin levels reaching those obtained during milking and by the effect of milk transfer from the alveolar to the cisternal lumen. Additionally, progesterone could act directly on milk synthesis at the level of the secretory cells.

Animals↗
PubMed1992

Angiotensin-converting enzyme inhibition and diabetic nephropathy.

Hypertension and diabetes mellitus are strongly associated conditions from epidemiologic, genetic, and pathophysiologic points of view. The prevalence of hypertension is high in patients with diabetes, and, conversely, many patients with essential hypertension are glucose intolerant. Proteinuria appears in 40-50% of patients with insulin-dependent diabetes mellitus and 20-30% of patients with non-insulin-dependent diabetes mellitus. Progressive renal failure occurs in 30-40 and 3-8% of patients, respectively, hypertension being a leading factor in its rate of progression. In various animal experiments, ACE inhibitors are able to prevent proteinuria and glomerular sclerosis, presumably by lowering transglomerular capillary pressure. In the diabetic human, ACE inhibitors are powerful antihypertensive drugs, devoid of metabolic side effects. Clinical studies indicate that ACE inhibitors reduce proteinuria and possibly slow the rate of decline in renal function. Such an effect is not observed with beta-blockers. Large-scale studies are needed to confirm this very important hypothesis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Arterial hypertension in pregnancy. Role of maternal and fetal blood velocimetry].

Gravidic hypertension remains one of the most frequent causes of perinatal mortality and morbidity. There are two aims when investigating this disease: evaluate the gravity, try to find early signs of a risk of pre-eclampsia. This last point has become particularly important over the past few years because of the development of preventive treatment (platelet anti-agregates). Mother and fetal blood velocimetry play a more and more important role. Three measurement sites appear to have different and complementary importance: for long-term prediction, measuring the velocimetric index of the uterin artery seems the most interesting because it schematically explores the type of placentations; for mid-term, measuring the ombilical artery evaluates placenta resistance, an essential factor in chronic fetal suffering; at short-term, measuring the fetal cerebral and carotid vessels explores the hemodynamic reactions of fetal adaptation to fetal suffering.

Adult↗
PubMed1991

Prevention of fetal growth retardation with low-dose aspirin: findings of the EPREDA trial.

The efficacy of low-dose aspirin in preventing fetal growth retardation was tested in a randomised, placebo-controlled, double-blind trial. A secondary aim was to find out whether dipyridamole improves the efficacy of aspirin. 323 women at 15-18 weeks' amenorrhoea were selected at twenty-five participating centres on the basis of fetal growth retardation and/or fetal death or abruptio placentae in at least one previous pregnancy. They were randomly allocated to groups receiving placebo, 150 mg/day aspirin, or 150 mg/day aspirin plus 225 mg/day dipyridamole, for the remainder of the pregnancy. In the first phase of the trial all actively treated patients (n = 156) were compared with the placebo group (n = 73). Mean birthweight was significantly higher in the treated than in the placebo group (2751 [SD 670] vs 2526 [848] g; difference 225 g [95% CI 129-321 g], p = 0.029) and the frequency of fetal growth retardation in the placebo group was twice that in the treated group (19 [26%] vs 20 [13%]; p less than 0.02). The frequencies of stillbirth (4 [5%] vs 2 [1%]) and abruptio placentae (6 [8%] vs 7 [5%]) were also higher in the placebo than in the treated group. The benefits of aspirin treatment were greater in patients with two or more previous poor outcomes than in those with only one. In the second analysis, of aspirin only (n = 127) vs aspirin plus dipyridamole (n = 119), no significant differences were found. There was no excess of maternal or neonatal side-effects in the aspirin-treated patients.

Adult↗
PubMed1991

[Physiopathological elements of pre-eclampsia and the role of the main complementary tests].

The origin of pre-eclampsia lies in uteroplacental ischemia due to an anomaly of the "vascular insertion" of the placenta. Although the cause of this anomaly remains unknown, it would appear to include both a genetic and an immunological origin possibly favourised by special underlying conditions and certain obstetric circumstances. Prostaglandin imbalance (in particular prostacyclins and Thromboxane A2) appears to be one of the chief factors governing these anomalies. One of the consequences of these mechanisms is the onset of hypertension but other disturbances are essential features. In particular, disseminated intravascular coagulation may occur leading to the release of numerous microthrombi which cause placental (leading to chronic fetal distress), renal, hepatic and cerebral lesions.

Disseminated Intravascular Coagulation↗
PubMed1990

[Controlling hypertension in the pregnant diabetic woman].

High blood pressure occurs in many pregnant diabetic patients (30 to 40 p cent), and it is associated with significant impairement of fetal prognosis. Hypertension is no doubt a marker of the vascular diabetic disease, which obviates an adequate placentation. Proper antihypertensive management is necessary in those patients, but its prognostic importance is far less than is that of a perfect glycemic control. Antihypertensive therapy differs in some aspects from what is should be in non-pregnant patients: first, compounds such as angiotensin converting enzyme inhibitors, or calcium-channel blockers are not considered safe in pregnant women, whereas they are the first choice in non-pregnant diabetics. Second, over-control of blood pressure is very harmful to fetal growth, and should be carefully avoided. Finally, present literature lacks proper controlled studies, which could help in designing the best antihypertensive therapeutic strategy in pregnant diabetic patients.

Female↗
PubMed1990

[Attempts to prevent intrauterine growth retardation using platelet anti-aggregants].

Intrauterine underdevelopment is a frequent complication in pregnancies associated with high blood pressure. It can also happen in the absence of this symptom but in a similar context. During these pregnancies, homeostasis problems were often shown to be at the root of placental abnormalities responsible for the development problems. This is why the authors of this article have tried to prevent intrauterine underdevelopment by prescribing antiplatelet drugs as from the start of the 2nd trimester of pregnancy. They compare their encouraging results with those of other teams and conclude that a larger prospective trial is necessary.

Female↗