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Biomedical subjects

M Renard

Publications and source records attributed to M Renard.

At least 73 records · Page 4Linked to original sources
PubMed1994

Increased bone marrow toxicity of doxorubicin bound to nanoparticles.

The in vivo myelosuppressive effects of free and polyalkylcyanoacrylate-bound doxorubicin were compared in a mouse model. After intravenous administration of 11 mg/kg body weight of doxorubicin either free or bound to polyisobutyl (doxo-PIBCA) or polyisohexylcyanoacrylate (doxo-PIHCA) nanoparticles, we studied the total and differential counts of blood, bone marrow and spleen cells; the number of granulocyte progenitors (CFU-GM) was determined by culture. Doxorubicin concentrations were measured with an HPLC method in the bone marrow and the spleen. Doxo-PIHCA nanoparticles showed the highest and longest myelosuppressive effects which correlated well with a high concentration of the drug in the bone marrow and the spleen. Moreover, it was found that PIHCA nanoparticles induced the release of colony stimulating factors, which might account for the observed increase of toxic effects of doxorubicin on bone marrow progenitors. These data also indicate that a more precise evaluation of the myelosuppressive effects of targeted formulations of anticancer drugs is needed, which may be attained by studies on bone marrow progenitors.

Animals↗
PubMed1994

Role of growth hormone (GH)-releasing hormone and somatostatin in the mediation of clonidine-induced GH release in sheep.

GH secretion is stimulated by the administration of an alpha 2-adrenergic agonist, clonidine, in several species, including man. This action is probably mediated at the level of the hypothalamus, where the drug may act through inhibition of somatostatin (SRIH) and/or stimulation of GH-releasing hormone (GHRH) release. We have investigated the mode and site of action of clonidine in sheep, because it is possible to collect hypophysial portal blood for the simultaneous determination of GHRH and SRIH in this species under conscious unstressed conditions. Clonidine injection (0.3 mg, iv) resulted in a significant, immediate, and short-lasting (30-min) increase in peripheral GH (14.4 +/- 3.1 vs. 4.8 +/- 1.1 ng/ml; P < 0.01) and portal GHRH (2.7 +/- 0.5 vs. 1.0 +/- 0.2 pg/min; P < 0.01) levels. No change in SRIH secretion was recorded during the same period. Next, we tested the effect of clonidine in sheep actively immunized against GHRH or SRIH. The alpha 2-adrenergic agonist did not affect GH secretion in the anti-GHRH group, whereas immunization against SRIH did not modify the GH response. Finally, we observed that clonidine did not influence GH release from cultured ovine pituitary cells. These data suggest that clonidine acts centrally to stimulate hypophysial GH secretion in the sheep and that this effect is mediated through changes in GHRH, but not SRIH, release into hypophysial portal blood.

Animals↗
PubMed1994

Growth hormone (GH)-releasing hormone secretion is stimulated by a new GH-releasing hexapeptide in sheep.

The acute effect of a new GH-releasing peptide, hexarelin (1 mg, iv), on GH secretion and the mechanisms involved in its changes were investigated in conscious sheep. Peripheral GH levels and GH-releasing hormone (GHRH) and somatostatin concentrations in hypophysial portal blood were measured in six rams. An increase in jugular GH levels was observed 15 min after hexarelin injection (9.1 +/- 1.8 vs. 3.9 +/- 0.8 ng/ml; P < 0.05). This was associated with a stimulation of GHRH release into hypophysial portal blood (145.4 +/- 19.9 vs. 59.2 +/- 10.8 pg/ml; P < 0.01) without a change in somatostatin secretion. Our data indicate that GH-releasing peptide-induced GH stimulation in the sheep involves an activation of GHRH neurons in addition to the previously demonstrated direct effect on the pituitary cells.

Animals↗
PubMed1994

Blockade of alpha 2-adrenoceptors stimulates basal and stress-induced adrenocorticotropin secretion in the developing rat through a central mechanism independent from corticotropin-releasing factor and arginine vasopressin.

In the neonatal rat, the response of the hypothalamo-pituitary-adrenal axis to stressful stimuli is markedly reduced during the first 2 weeks of life [stress-hyporesponsive period (SHRP)]. In this report, we studied the effect of idazoxan (an alpha 2-adrenergic antagonist) on plasma ACTH and corticosterone levels in 8-day-old rats. Indeed, it is known that in the adult rat, blockade of alpha 2-adrenoceptors increases ACTH secretion stimulated by CRF and arginine vasopressin (AVP) injection. Injection of 2.5 micrograms/g idazoxan induced a rapid (within 30 min) increase in basal plasma ACTH and corticosterone levels that lasted for 60 min. Injection of increasing doses of idazoxan led to a dose-dependent stimulation of ACTH and corticosterone levels. Administration of 2.5 micrograms/g idazoxan significantly increased the ACTH response to insulin-induced hypoglycemia, whereas it potentiated and accelerated the ACTH response to ether exposure stress. We next examined ACTH secretion from superfused anterior pituitary glands. Neither the alpha 2-adrenergic agonist clonidine nor idazoxan changed the basal ACTH secretory rate. Idazoxan had no effect on CRF- and AVP-stimulated ACTH secretion. This indicates that in vivo, idazoxan acts at a suprapituitary level. To investigate a possible effect of idazoxan on presynaptic alpha 2-adrenoceptors, we studied the effect of idazoxan on the concentrations of norepinephrine (NE) and L-DOPA in punches of locus coeruleus after dopa-decarboxylase blockade. Idazoxan injection induced a decrease in the NE content, without changing L-DOPA levels, indicating that idazoxan can act at the level of presynaptic alpha 2-adrenoceptors, inducing an increased release and/or degradation of NE without any effect on catecholamines synthesis. Finally, we investigated a possible involvement of CRF and AVP in mediating the effect of alpha 2-adrenoceptor blockade on ACTH secretion. Passive immunization against CRF or AVP did not change the ACTH response to idazoxan administration, whereas idazoxan pretreatment had simply an additive effect on CRF- and lysine vasopressin-stimulated ACTH secretion. In conclusion, our data demonstrate that during the SHRP, blockade of alpha 2-adrenoceptors induces an increase in both basal and stress-induced ACTH secretion. They suggest that a decreased catecholaminergic tone, consecutive to an increased occupation of alpha 2-adrenoceptors, acting through a central mechanism independent from CRF and AVP may be responsible for the SHRP in the developing rat.

Adrenergic alpha-Antagonists↗
PubMed1993

Separation of red blood cells by field flow fractionation.

Field flow fractionation (FFF) is a new methodology described as being well-suited for the separation and characterization of biopolymers and particles. On theoretical grounds, cells may be separated with FFF if they differ in size, density or deformability. In the present study, we first tried to determine optimal separation conditions for red blood cells; thereafter we used FFF to examine red cell changes during a phenylhydrazine-induced hemolytic anemia. It has been shown that in less than 30 minutes, FFF is able to separate normal red blood cells from Heinz body-rich cells or reticulocytes that differ in size or density. The successive steps of hemolysis and regeneration appear clearly on the fractograms. Advantages and drawbacks of the method are discussed.

Anemia, Hemolytic↗
PubMed1992

Influence of upright exercise on pulmonary hemodynamics in left heart failure.

Studies in severe chronic stable heart failure (HF) indicate that pulmonary resistance might remain unchanged during exercise and could subsequently contribute to limitation in exercise capacity of these patients. We assessed the possible role of the exercise decreases in mixed venous oxygen tension on this phenomenon in fifteen patients with chronic congestive heart failure (N.Y.H.A. functional classes II to IV) who underwent a symptom-limited treadmill exercise test with hemodynamic monitoring as well as repeated arterial and mixed venous blood gas analysis. For all patients there was an increase in cardiac output (from 3.7 +/- 0.2 to 6.7 +/- 0.5 l/min, p less than 0.001) and pulmonary wedge pressure (from 16 +/- 2 to 31 +/- 3 mm Hg, p less than 0.001) along with exercise with highly significant decrease in total systemic resistance and no significant (from 25.6 +/- 1.5 to 15.8 +/- 1.0 U, p less than 0.001) changes in pulmonary vascular resistances. Arterial blood oxygen tension increased from 86 +/- 3 to 99 +/- 3 mm Hg (p less than 0.001) and mixed venous oxygen tension (PvO2) decreased from 33 +/- 1 to 22 +/- 1 mm Hg (p less than 0.001). Changes in pulmonary vascular resistance during exercise were inversely related to changes in PvO2 (r = -0.61; p less than 0.05). We conclude that the observed decrease in PvO2 might be a determinant of unchanged pulmonary vascular resistance during treadmill-exercise test in severe heart failure patients.

Adult↗
PubMed1991

Developmental hematopoiesis in normal human fetal blood.

Using an easy and safe procedure for fetal blood sampling in utero, we studied 3,415 fetuses for prenatal diagnosis. Retrospectively, 2,860 normal blood samples, performed from the 18th week of gestation to the end of pregnancy, were selected. Differentials were evaluated in 732 cases. Burst-forming unit erythroid (BFU-E) and erythropoietin (Epo) were measured in 27 and 163 cases, respectively. Total nucleated cell and platelet counts did not change from the 18th to the 30th week of gestation. The lymphocytes represented the main population and the decrease of normoblastic cells made up for the increase in neutrophils. The increase of red blood cells and hemoglobin was substantial during the studied period. At mid trimester threefold more BFU-E were obtained than at birth. Epo levels remained stable throughout the pregnancy and no correlation was found between Epo and gestational age. These normal values of fetal erythropoiesis will improve our knowledge of physiology and provide a better insight into developmental hematopoiesis.

Adult↗
PubMed1991

Infantile fibrosarcoma.

Explore the source record for details and available documents.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Striatal proenkephalin turnover and gene transcription are regulated by cyclic AMP and protein kinase C-related pathways.

Preproenkephalin metabolism, in the rat, was studied in primary striatal neurons maintained in a chemically defined medium. Acute treatment (30 min) with forskolin (10(-5) M) or phorbol 12 myristate 13 acetate (10(-7) M) resulted, respectively, in a two- and seven-fold increase in methionine-enkephalin secretion. Chronic treatment with forskolin or phorbol 12 myristate 13 acetate (24 h) induced a 100% increase in methionine-enkephalin content (forskolin) and on the other hand a 50% decrease in methionine-enkephalin (phorbol 12 myristate 13 acetate). Both treatments increased preproenkephalin mRNA levels in a time-dependent manner, this augmentation being observable after 180 min by Northern blot analysis and in situ hybridization. These data indicate that under chronic stimulation, with either forskolin or phorbol 12 myristate 13 acetate, proenkephalin turnover is accelerated. However, after stimulation with phorbol 12 myristate 13 acetate, the more potent methionine-enkephalin secretagogue, increased peptide synthesis is not sufficient to replenish methionine-enkephalin intracellular stores. Preproenkephalin gene transcription was analysed by introducing the preproenkephalin gene promoter fused to the bacterial acetyl chloramphenicol transferase reporter gene into primary neurons. Chronic stimulation (48 h) by forskolin (10(-5) M) or phorbol 12 myristate 13 acetate (10(-7) M) of striatal neurons transfected with this fusion gene increased chloramphenicol acetyltransferase activity six-fold and the two effects were additive. These data suggest that the cyclic AMP and the protein kinase C pathways directly activate preproenkephalin gene transcription.

Animals↗
PubMed1991

[Activity of the sympathetic nervous system and of the renin-angiotensin system in the acute stage of myocardial infarction].

We studied sympathetic and renin-angiotensin systems activity in a series of 175 patients suffering from acute myocardial infarction. These two systems were both overactivated especially in the cases complicated by hemodynamically documented left heart failure. The response of these systems to acute heart failure was in the same range for patients younger or older than 65 years and the witness (norepinephrine and plasma renin levels) of sympathetic and renin-angiotensin activities were good independent prognostic factors of in-hospital mortality.

Acute Disease↗
PubMed1991

Cervical cord compression in scleroderma. One case.

The cervical spine is rarely involved in scleroderma. The lesions reported here consisted of osteolysis of the posterior arches disturbing vertebral statics, and exuberant calcifications responsible for spinal cord compression by stenosis of the vertebral canal.

Calcinosis↗
PubMed1991

Erythropoietic progenitor cells in human fetal blood.

Ultrasound guided fetal blood sampling performed for diagnostic purposes allowed us to determine the circulating level of erythropoietic progenitor cells (BFU-E) from the 19th to 30th weeks of gestation. Normal fetal blood showed a mean of 160 BFU-E (+/- 107) per 10(5) nucleated cells during the second and third trimesters of pregnancy, which is 3 times higher than in cord blood at birth and 10 times higher than in adult bone marrow. These findings are in keeping with an important circulation of hematopoietic progenitors during fetal life.

Adult↗
PubMed1990

[Refractory arterial hypoxemia and interatrial right-left shunt in myocardial infarction of the right ventricle].

The authors report the case of a 63 year old woman who developed refractory arterial hypoxemia due to a right-to-left interatrial shunt through a patent foramen ovale during the acute phase of right ventricular infarction. The precarious haemodynamic condition of the patient contra-indicated surgical intervention and so the effects of the shunt were reduced by obstructing the atrial septal defect with the balloon of a Swan-Ganz catheter. The management of this type of shunt is discussed based on the degree of hypoxemia and the patient's haemodynamic status with reference to this particular case and a review of the literature.

Catheterization, Swan-Ganz↗
PubMed1990

[Thrombolysis in the acute stage of myocardial infarction].

The authors recall the conditions in which intravenous thrombolysis is justified, and the mode of action of the various thrombolytic products. They show the efficacy and the utility of thrombolysis and also its complications. The success of this treatment is closely linked to the time interval after thrombosis, which should be reduced as much as possible.

Fibrinolytic Agents↗
PubMed1990

[Hemodynamic impact of pressotherapy].

We study the hemodynamic effects of pressotherapy in 11 patients (mean age : 68 +/- 10 years) with uncomplicated acute myocardial infarction (n = 6) or with chronic ischemic heart failure (n = 5). We measure the right auricular pressure (RAP), the mean pulmonary arterial pressure (MPAP) and the pulmonary wedge pressure (PWP), before, during pressotherapy (MPAP) and the pulmonary wedge pressure (PWP), before, during pressotherapy (T 20 min) and 30 minutes after the end of pressotherapy (T 30 min). We use five-chambered leg garments with 80 mm Hg pressure during 20 minutes. The wavelike action (from the bottom to the top) is intermittent: the compression time is 10 second (sec); compression is maintained during 60 sec; deflation time is 15 sec. After 20 minutes pressotherapy (t 20) the 3 variables increase: RAP: from 3.6 +/- 5 to 7 +/- 7 mm Hg (P less than 0.001), MPAP: from 25 +/- 14 to 29 +/- 17 mm Hg (p less than 0.01) and the PWP from 10 +/- 8 to 17 +/- 11 Hg (p less than 0.01). This rise is particularly important in heart failure patients: from 18 +/- 8 to 29 +/- 8 mm Hg for the PWP, with cough in one patient. At T 30 these 3 variables decrease and return nearly to initial values: respectively 2.7 +/- 4.7 (RAP), 24 +/- 14 (MPAP), 12 +/- 8 mm Hg (PWP). In conclusion pressotherapy increases RAP and pulmonary pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

[Short- and long-term prognosis of myocardial infarct. Contributions and limitations of the clinical aspects and non-invasive technics].

Clinical variables and those obtained by non-invasive techniques were recorded in a series of 306 patients discharged from hospital after an acute myocardial infarction. We studied the prognostic value at 2 and 12 months of these variables (alive/dead). The results of simple clinical data were as discriminant as those from more elaborated techniques. When the prognostic value of the same data at 12 months was studied in those surviving for two months, most of the predictive variables lost their discriminant power. The study shows that the predictive value of many of the predischarge variables usually taken into account in the assessment of long term risk, does not extend beyond the first two months.

Echocardiography↗