[Isotopic detection of malignant bone tumors].
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Biomedical subjects
Publications and source records attributed to R Moreau.
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A decrease in plasma noradrenaline--a reflection of sympathetic nervous system activity--by clonidine, a centrally acting alpha 2-agonist, could reduce the hyperdynamic circulation observed in cirrhosis and may thereby decrease portal hypertension. Plasma noradrenaline concentration and plasma renin activity as well as systemic and splanchnic hemodynamics were measured in 12 patients with cirrhosis and ascites before and after administration of either 150 micrograms of clonidine or placebo. Plasma noradrenaline concentration significantly decreased in all patients after clonidine administration, whereas plasma renin activity did not change significantly. There were statistically significant reductions of cardiac output (-17.4%), mean arterial pressure (-12.2%), hepatic venous pressure gradient (-19.7%) and azygos blood flow (-26.6%) after administration of clonidine. No significant correlation was found between the reduction of plasma noradrenaline concentration and changes in systemic or splanchnic hemodynamics. Hepatic blood flow was not changed by clonidine. Placebo administration had no effect on any laboratory or hemodynamic measurement. We conclude that the reduction in sympathetic nervous system activity by clonidine and the subsequent decrease in the hyperdynamic circulation suggests that sympathetic overactivity contributes to the circulatory derangements in patients with cirrhosis.
We studied the acute effects of ketanserin, a serotonin S2 antagonist, on systemic and splanchnic hemodynamics in 11 patients with cirrhosis. Mean arterial pressure decreased moderately but significantly after ketanserin. This effect was maximal at 5 min and correlated to the severity of cirrhosis. Cardiac index and systemic vascular resistance were not significantly changed. The hepatic venous pressure gradient, used as an index of portal pressure, significantly decreased after ketanserin (-23%). Azygos blood flow, a reflection of superior portosystemic collateral blood flow, also significantly decreased (-26%), but this effect was delayed, progressive and not correlated to the arterial pressure decrease. Hepatic blood flow was unchanged. These findings suggest that the systemic and splanchnic circulations may be hypersensitive to ketanserin in cirrhotic patients, and that serotonergic mechanisms may contribute to maintain portal hypertension. New specific antiserotonergic drugs deserve further evaluation for potential therapeutic implications in portal hypertension.
The hemodynamic response to a 800 kcal liquid meal was investigated in 24 patients (study group) with cirrhosis and two control groups. One control group of six cirrhotic patients (volume control) had a calorie-free equivolumic electrolyte solution. The second control group (normal control) of six patients with normal hepatic function had the same test meal. Cardiac index, mean arterial pressure, heart rate, hepatic venous pressures, hepatic blood flow and azygos blood flow (only measured in the study group) were measured before and 30 and 60 min after the meal. Systemic circulatory responses were generally absent. Hepatic blood flow and wedged hepatic venous pressure increased significantly in both cirrhotic patients and normal controls; however, cirrhotic patients tended to have a quicker response (peaks at 30 min) than normals (peaks at 60 min). Azygos blood flow showed large postprandial variability, but overall did not change significantly. These results demonstrate that the splanchnic circulation of the patient with cirrhosis reacts differently from normals to the physiologic stimulus of a meal, and in particular appears to have precocious vasoactive reactivity.
To delineate the circulatory effects of glucagon in cirrhosis, we infused two moderately supraphysiological doses of this hormone into 19 patients with cirrhosis and determined hemodynamic responses. Patients were divided into a group with good liver function (Pugh Class A, n = 8) and poorer function (Pugh Class B and C, n = 11). All patients received glucagon at 10 ng per kg per min for 20 min, then 20 ng per kg per min for a further 20 min. These doses raised serum glucagon levels to a similar degree in both groups of patients. Serum glucose levels also rose in both groups but to a lesser degree in Class BC patients. Serum noradrenaline and adrenaline remained unchanged in both groups. Heart rate, mean arterial pressure, cardiac index, systemic vascular resistance, hepatic venous pressure gradient and hepatic blood flow were measured basally and during the second glucagon infusion. None of these measurements significantly changed in either group of patients. Azygos and renal venous blood flow were measured basally and during the first and second infusions. Azygos flow increased significantly only in Group A patients: basal, 0.32 +/- 0.03 liter per min; first infusion, 0.40 +/- 0.06 liter per min; second infusion, 0.49 +/- 0.07 liter per min. Corresponding values in Group BC patients were: 0.54 +/- 0.08, 0.54 +/- 0.08 and 0.52 +/- 0.08 liter per min. Renal blood flow did not change significantly. One patient with a portacaval shunt increased superior mesenteric venous flow from 0.78 liter per min to 0.95 liter per min with glucagon.(ABSTRACT TRUNCATED AT 250 WORDS)
Placental transfer of maternal calcium (Ca(2+)) is a crucial process for fetal development although the biochemical mechanisms responsible for this transfer are largely unknown. We have investigated the characteristics of Ca(2+)uptake by the human placental trophoblast cell line BeWo. The kinetics studies revealed an active extracellular Ca(2+)uptake by BeWo cells, which was rapid in the first 2 min (initial velocity (V(i)) of 4.17+/-0.25 nmol/mg/min), and showed a subsequent plateau. Uptake experiments performed at V(i)with increasing concentrations of Ca(2+)resulted in a typical saturation curve (K(m)of 0.54+/-0.07 m m and V(max)of 7.07+/-0.28 nmol/mg protein/min). Lowering the pH of the incubation medium from 7.4 to 5.5 led to Ca(2+)uptake inhibition of 40-50 per cent. The presence of voltage-sensitive (l -type) Ca(2+)channels in BeWo cells was demonstrated by Western blot. Therefore, the implication of such channels in basal Ca(2+)uptake of BeWo cells was investigated. Cell depolarization with extracellular high potassium concentration (40 m m), and hyperpolarization with extracellular high chloride concentration (60 m m) or with valinomycin (10 microm) did not influence the basal Ca(2+)uptake of BeWo cells. The L-type Ca(2+)channel modulators (Bay K 8644 and Nitrendipine) had no effect on the Ca(2+)uptake. An antagonist of receptor-mediated, store-operated and voltage-gated Ca(2+)channels (SKF-96365) also did not modulate the Ca(2+)uptake of BeWo cells. Therefore, our results indicate that the basal Ca(2+)uptake of BeWo cells is inhibited by lowering pH of the incubation medium, is voltage independent, and is not influenced by l -type Ca(2+)channel and capacitative Ca(2+)conductance modulators.
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The author describes two cases of bone changes following non-intra-articular and more probably sub-chondral injection of corticosteroids. The first, in condyle a mandibular was reversible with reconstruction of the bone after a year. The second, in the condyle of a knee was definitive with a permanent chip in the bone.
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