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Biomedical subjects

H Michel

Publications and source records attributed to H Michel.

At least 361 records · Page 20Linked to original sources
PubMed1978

Effect of prostacyclin (PGI2) on platelet adhesion to rabbit arterial subendothelium.

The effect of prostacyclin on platelet aggregation and adhesion was investigated in everted pieces of rabbit abdominal aorta, from which the endothelium had previously been removed. Citrated human blood, to which different, concentrations of prostacyclin (0.1-100 ng/ml) were added, was perfused through the vessels, after which sections were examined and evaluated by light microscopy. Prostacyclin inhibited thrombus formation at concentrations greater than 0.1 ng/ml, whereas 20 ng/ml were required to reduce the amount of adhesion to the subendothelial surface. Thus prostacyclin prevents thrombus formation at much lower concentrations than are needed to inhibit platelet-vessel wall interaction.

Animals↗
PubMed1977

[Lateral transparietal cholangiography. Okuda's technic. Remarks apropos of 111 examinations].

The diagnosis of proctated jaundice is done in 50% of all cases by clinical examination; in 30% of all cases by peritoneoscopy; in the other 20% instrumental opacification of the biliary tract is required (before the laparotomy) in order to determine the site and the nature of the cholestasis. Among these instrumental devices, a transhepatic cholangiography with the Okuda needle allows biliary tract opacification in 98% of all cases if the obstacle is extra-hepatic and in 69% of all cases if the obstacle is intra-hepatic. This technique is easy to perform, without danger, and readily available to any physician. It should be performed after the peritoneoscopy and before the retrograde cholangiography.

Bile Ducts, Intrahepatic↗
PubMed1977

Adhesion and aggregation of human platelets to rabbit subendothelium. A new approach for investigation: specific antibodies.

An SgG antibody occurring in a recently transfused thrombasthenic patient inhibited all the ADP-mediated aggregations and platelet-platelet interaction (thrombus formation) on rabbit aorta subendothelium; another IgG antibody occurring in a multitransfused Bernard-Soulier patient inhibited ristocetin and bovine factor VIII mediated aggregation and platelet-subendothelium interaction.

Animals↗
PubMed1977

[Hepatic encephalopathies; hemodynamic and metabolic study of the influence of ammonia and levodopa].

The authors present the results of a study of cerebral blood flow and energy metabolism carried out in 19 subjects, 12 of whom had hepatic cirrhosis and hepatic encephalopathy (HE). The spontaneous changes and those noted after intravenous administration of ammonium chloride and of L. Dopa, shows that the signs of hepatic encephalopathy are not directly related to the reduction in energy metabolism and that this metabolic disorder does not depend on a blocking of the dopaminergic synopses. The results of this study emphasize the complexity of HE and raise up the hypothesis of the creation of intra-cerebral arterio-venous shunts in cirrhotic patients.

Ammonia↗
PubMed1976

[Platelet anomaly in an eosinophilic myelophroliferative syndrome].

The authors report a case of chronic eosinophilic leukemia. Ristocetin did not aggregate patient's platelets in the absence of bleeding disorder. A possible relationship between arterial thrombosis observed in patients with eosinophilic leukemia and platelet abnormality is evoked.

Arteries↗
PubMed1976

Relation between the inhibition of aggregation and the concentration of cAMP in human and rat platelets.

Adenosine inhibits the aggregation of human but not of rat platelets whereas both are inhibited by prostaglandin E1 or by the pyrimido-pyrimidine compound RA233. In human platelets all three agents increase adenosine-3'-5'-cyclic monophosphate (cAMP). If the inhibition of aggregation depended on this increase, adenosine might be expected not to increase cAMP in rat platelets. Under conditions in which adenosine inhibited aggregation and increased cAMP in human platelets, adenosine caused a similar increase in cAMP in rat platelets without inhibiting their aggregation. The aggregation of rat platelets was inhibited as effectively as that of human platelets by PGE1 or RA233 at concentrations which caused greater increases in cAMP than did the highest concentrations (2.8 X 10(-4) M) of adenosine it was possible to use. When the increase of cAMP in rat platelets by PGE1 was limited to that produced by adenosine, PGE1 like adenosine failed to inhibit aggregation. Therefore, the difference in the inhibitory effectiveness of adenosine on rat and human platelets was quantitative rather than qualitative and apparently depended on the inability of adenosine to increase cAMP sufficiently in rat platelets. When cAMP had been increased by adenosine, PGE1 or RA233, the addition of ADP caused cAMP to decrease rapidly in both human and rat platelets to between +22 and -18% of control values, except that the decrease in rat platelets was to +40% after RA233 had been present for 0.5 min before ADP. The increase in cAMP produced in rat platelets by adenosine at 5 X 10(-6) to 2.8 X 10(-4) M for 3 min was associated with a small increase in aggregation velocity. It is suggested that the comparative ineffectiveness of adenosine as an inhibitor of platelet aggregation, particularly with rat but less so also with human platelets, is because, unlike PGE1 or RA233, adenosine has two opposing actions on aggregation; one being inhibition by activating adenylate cyclase and increasing cAMP, and the other being potentiation by uptake. This hypothesis accounts for the present results as well as for the earlier observation that dipyridamole which prevents the uptake of adenosine potentiates its inhibitory effect on the aggregation of human platelets.

Adenosine↗
PubMed1976

[Rise in incidence of pulmonary embolism fatalities among surgical patients and disposing factors involved. Analysis for a 50 year period (author's transl)].

During the 50 year period from 1917 to 1966, 210078 patients were treated in the Surgical Clinic of the University of Jena. Autopsies were carried out on 10083 of the patients which had dies in the Clinic. The average incidence rate of lung embolism was 0.44%, the range of values lying between 0.04% (1917) and 1.02% (1965). In periods of famine or distress, lung embolism reached its lowest point, whereas in periods of relative prosperity a high peak was reached. On the whole, the incidence of pulmonary embolism seem to be the increased age of the patients population and the higher frequency of associated heart and circulatory diseases, obesity, and accidents, as well as the extended indications for surgery in the aged.

Adult↗
PubMed1976

Bernard-Soulier syndrome: a new platelet glycoprotein abnormality. Its relationship with platelet adhesion to subendothelium and with the factor VIII von Willebrand protein.

A decreased platelet adhesion to rabbit aorta subendothelium (Baumgartner technique) is confirmed in the Bernard Soulier (giant platelet) syndrome. Electron microscope techniques using a purified antibody against Factor VIII/von Willebrand protein, revealed an apparently normal presence of the Factor VIII/von Willebrand protein on the Bernard Soulier platelets. Electrophoretic characterization of the major protein and glycoprotein components of the Bernard Soulier platelets following sodium dodecyl sulfate solubilization indicated a relatively normal protein content but suggested a reduced content of the 155,000 molecular weight major platelet glycoprotein. This was confirmed by a reduced release of high molecular weight acidic glycopeptides following incubation of washed Bernard Soulier platelets with trypsin. It is proposed that this abnormality may be related to the previously reported reduced sialic acid content and the reduced electrophoretic mobility of the Bernard Soulier platelets and that a glycoprotein reduced or abnormal in the Bernard Soulier platelets is necessary for the normal adhesion of platelets to subendothelium.

Adult↗
PubMed1976

Management of acid-peptic esophageal strictures.

Eighty-nine patients with benign acid-peptic strictures of the esophagus were evaluated. Of these, 56 patients were treated by dilatation and medical therapy, whereas 33 underwent operative therapy because medical therapy failed. Three patients, all psychotic and having post-emetic strictures, required resection of the stricture and a colon interposition. Twenty-nine patients underwent a Belsey or Nissen fundoplication combined with esophageal dilatation. Fourteen of 29 had an associated vagotomy and 15 did not. Two patients of this 29 had a poor result, one of whom had a post-emetic stricture. Although the patients having a concurrent vagotomy and pyloroplasty had the more severe disease,there was no significant difference between the results in the two groups. It is concluded that most patients with such esophageal strictures may be adequately treated without resecting the stricture and that the routine addition of a vagotomy and drainage procedure is probably not indicated.

Aged↗