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Biomedical subjects

P Labrude

Publications and source records attributed to P Labrude.

99 records · Page 6Linked to original sources
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The Strasbourg's pharmacy school transfer to Nancy (October the 1st, 1872).

After a short history of the High school of pharmacy of Strasbourg and of the school of medicine and pharmacy of Nancy, and their situation in 1870, the author describes the modalities of the transfer concerning pharmacy. The first years in Nancy and the difficulties due to the existence of military fellows and to vacancy of two chairs are evocated here. The names of numerous teachers are given. The paper continues about the autonomy of the school in 1876, with the professors nominated at the chairs, with the extension of buildings and increase of students. Despite of early difficulties encountered during the settling in Nancy, it appears that the transfer from Strasbourg was a success and the school of pharmacy found rapidly its place inside the great University created in Nancy after the war.

France↗
PubMedDate not supplied

[Relationship between arterial pressure evolution and free hemoglobin distribution into vascular wall in guinea pigs].

Free hemoglobin (Hb) present at high concentration in plasma--in case of hemolysis, hemoglobin based oxygen carrier (HBOC) administration or in case of subarachnoid hemorrhage--induce hypertension as result of vasoconstriction. In this context, we studied on an exchange transfusion (ET) model at 50% of hematocrit with a HBOC, the distribution of this Hb inside abdominal aortic wall in guinea pigs in relation with mean arterial pressure (MAP) evolution. MAP was monitored during 180 min after ET and rings of abdominal aorta were taken at different times, when modifications of MAP were important, and analyzed by immunohistochemistry and confocal microscopy. Gelofusine 4%, used as control, did not modify MAP while free Hb increased MAP that reached its maximum (53% of hypertension) at t=17 min after the end of ET. MAP started to decrease (45% of hypertension) at t =60 min after ET, and recovered its baseline value at t=180 min. Confocal analysis of the vessel showed that: at 17 min (when hypertension was maximal), free Hb was present in endothelial cells (EC) and in vasa vasorum; at t=60 min (when hypertension decreased) and at t =10 min (when hypertension disappeared), free Hb was detected still in EC, but inside all abdominal aorta wall too. These results suggest in the first time that free Hb could induce a hypertension by direct interaction with EC but would also be unable to maintain this hypertension in spite of its massive tissue distribution.

Animals↗
PubMedDate not supplied

[Potential mechanism of dextran-conjugated hemoglobin penetration inside arterial wall].

Several reports indicated that cell-free hemoglobin induced vasoconstriction. This phenomenon was due to different pharmacological (NO trapping, vasoactive agents release and endothelial uptake...) and physical (viscosity and oxidative process of cell-free hemoglobin...) factors. We have previously showed that the blood pressure increase would be due to the presence of Dex-BTC-Hb inside arterial wall. However, we do not know how hemoglobin penetrate inside arterial wall. The objective of this study was to examine the new hypothesis of hemoglobin penetration inside arterial wall dependent of endocytosis. For this reason, an endocytosis inhibitor, cytochalasin D, was tested. We measured in anesthetized guinea pigs, the evolution of mean arterial pressure (MAP) and plasma hemoglobin concentration in presence or absence of cytochalasin D (1.6 x 10(-4) M). These measurements were carried out before and after 50% isovolemic exchange transfusion (IET) with two cell-free hemoglobins: Dex-BTC-Hb (300 kDa) and stroma-free hemoglobin (64.5 kDa). The administration of Dex-BTC-Hb or stroma-free hemoglobin induced an immediate increase in MAP that peaked within 17 min after IET and returned to baseline after 120 min. cytochalasin D attenuated the elevation of MAP when administrated before Dex-BTC-Hb but not when administrated before stroma-free hemoglobin. Furthermore, without cytochalasin D, plasma hemoglobin concentration after Dex-BTC-Hb or stroma-free hemoglobin administration decreased significantly 120 min after IET. In presence of cytochalasin D, plasma hemoglobin concentration stayed constant in Dex-BTC-Hb-treated animals but not in stroma-free hemoglobin-treated animals. cytochalasin D inhibits the endocytosis in case of Dex-BTC-Hb but not in case of stroma-free hemoglobin. This would be due to the molecular weight of cell-free hemoglobin. Based on these data, we suggest that endocytosis is one of the mechanisms by which cell-free hemoglobin with high molecular weight penetrated inside vascular endothelial cells. This endocytosis would have an impact on induced hypertension.

Animals↗
PubMedDate not supplied

[The medicinal leech Hirudo medicinalis: clinical use of the animal and therapeutic prospects of hirudin].

Blood sucking leech, Hirudo medicinalis, used in Medicine for very long, knew an intensive employment during early 18e century but its excess was responsible of the temporary disparition of the animal from the therapeutics. Leech has currently recovered a clinical use, especially in microsurgery. On the other hand, hirudin, main active compound isolated from leech extract and also known and used for long, offers interesting outlooks by its anticoagulant and antithrombic properties. This explains the great interest of hirudin preparation by molecular genetics.

Animals↗
PubMedDate not supplied

[Systemic lupus erythematosus manifested by thrombophlebitis of the lower limbs].

The diagnosis of systemic lupus erythematosus was made in a 9 year old boy who had presented two months earlier with an extensive thrombosis of the inferior vena cava and femoral veins. Haemostatic abnormalities were detected as follows: a moderate thrombocytopenia, increased platelet aggregation and stickiness, and a circulating anticoagulant (antithromboplastin).

Blood Coagulation↗
PubMedDate not supplied

[Erythrocyte, plasma and substitute hemoglobins facing physiological oxidizing and reducing agents].

Oxidation of hemoglobin is constant and normal in red blood cells and in all biological media. The knowledge of the mechanisms which manage oxidation state is perhaps sufficient to treat acquired and some hereditary methemoglobinemia. But in case of transfusional treatment with hemoglobin based oxygen carrier (HBOC), some preclinical investigations on the oxidation of these products in vivo in plasma showed that our knowledge was not sufficient to understand and control all oxidations which could occur. This review analyses the literature on the different mechanisms in red blood cells and plasma by which hemoglobin autooxidizes and by which endogenous oxidizing agents or their precursors (nitric oxide, peroxynitrite, superoxide, hydrogen peroxide) could oxidize it. It shows the production of different radical or non-radical oxygen species during hemoglobin autooxidation and oxidation processes and the different physiological or accessory mechanisms that could prevent or reduce the various oxidizing states of hemoglobin (HbFe3+, HbFe4+) in blood. Plasma contains a few anti-oxidizing or reducing systems but it profits by antioxidizing and reducing activity from red blood cells. In blood, oxidation state of hemoglobin results from very complex phenomena and if the body struggles against methemoglobin formation to maintain oxygen transport, the oxidation of hemoglobin is sometimes useful to protect tissues against various and numerous endogenous radical or non-radical oxidizing agents. In blood, a balance between all these oxidizing and reducing mechanisms makes it possible to regulate circulating methemoglobin rate.

Antioxidants↗