[Tuberculous aneurysms of the hepatic artery--a rare cause of hemobilia].
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Biomedical subjects
Publications and source records attributed to C Schwarz.
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Endogenous prostaglandins have been reported to be essential for the inhibitory effect of somatostatin on acid secretion. From these results it could be suggested that the effect of somatostatin on the secretion of gastroentero-pancreatic hormones may also be medulated by prostaglandins. This hypothesis was investigated in man and in the rat. Somatostatin-induced inhibition of postprandial gastrin, cholecystokinin, pancreatic polypeptide, and insulin release was not influenced by indomethacin pretreatment in healthy subjects. Using the isolated perfused rat stomach preparation, inhibition of acetylcholine-stimulated gastrin secretion by somatostatin was found to be unchanged by indomethacin treatment. It is concluded that endogenous prostaglandins are unlikely to be indispensable for the inhibitory effect of somatostatin on gastroentero-pancreatic endocrine cells.
The dissociation of the extracellular hemoglobin of Tubifex tubifex at alkaline and acid pH, and its reassociation upon return to neutral pH, was investigated using gel filtration, ultracentrifugation, and polyacrylamide gel electrophoresis in sodium dodecyl sulfate (SDS-PAGE). Tubifex hemoglobin dissociated at pH above 8 and below 6; both dissociations appeared to be equilibrium processes. The extent of dissociation increased as the pH moved away from neutrality; although dissociation was virtually complete at pH 11, its extent at acid pH did not exceed 50-60% at pH 4. Ca(II), Mg(II), and Sr(II) cations over the range 1-100 mM decreased the extent of the dissociation only at alkaline pH. The visible absorption spectrum of the oxyhemoglobin remained unaltered in the pH range 4-9. At more extreme pH, it changed with time, altering irreversibly to that of the aquo ferri form. Gel filtration of the hemoglobin at both extremes of pH showed that it dissociated into two heme-containing fragments; one consisting of subunit 1 (Mr approximately 17,000) and the other containing subunits 2, 3, and 4 of the hemoglobin (Mr approximately 60,000). Upon return to neutral pH, the dissociated fragment reassociated to the extent of 50 to 80% to whole hemoglobin molecules. The reassociation decreased with increase in alkaline pH, and with decrease in acid pH to which the hemoglobin had been exposed; it increased in the presence of Ca(II), Sr(II), and Mg(II) only subsequent to dissociation at alkaline pH. The SDS-PAGE patterns, gel-filtration elution volumes, and alpha-helical contents, determined from circular dichroism at 222 nm, of the reassociated whole molecules were identical to those of the native hemoglobin.
Two chemically unrelated inhibitors of lipolysis were used in order to differentiate between the effect of FFA depression and a possible FFA-unrelated drug effect, respectively, on the plasma concentrations of GH, cortisol, and glucagon. Saline infusion served as a control experiment. In eight healthy male volunteers, a similar FFA depression by either iv infusion of nicotinic acid (3-pyridine-carboxylic acid, NA) or oral intake of an adenosine derivative, N(6)-allyl-N(6)-cyclohexyl-adenosine (AD-D), was followed by a significant GH increase (to 22.1 +/- 6.2 and 9.6 +/- 2.9 ng/ml at 240 and 270 min, respectively). Due to the large scatter of the GH concentrations during NA infusion, these responses were not significantly different. No GH increase occurred when the FFA depression was prevented by addition of a lipid infusion. In contrast, plasma cortisol and glucagon both increased significantly (by 107.4 micrograms/liter at 270 min and by 48.4 pg/ml at 60 min, respectively) during NA- but not during AD-D-induced FFA depression. Addition of the lipid infusion abolished the cortisol increase during NA infusion but had no influence on basal cortisol concentrations during AD-D intake. It lowered glucagon to values slightly below basal concentrations when added to the NA infusion and more markedly during AD-D administration. The results provide evidence that 1) depression of plasma FFA per se stimulates the secretion of GH, and 2) the increase of cortisol and glucagon during NA infusion is probably unrelated to the FFA depression. Hence, the stimulatory effect of FFA lack on glucagon secretion needs to be reconsidered.
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56 patients with acute ischemic cerebral infarction were randomly allocated to intravenous treatment for 6 days with either 500 ml of a 10% glycerol solution or 500 ml of a 5% dextrose solution (placebo). The neurological status of the patients was evaluated by a blinded investigator before the beginning of the treatment, after 2 weeks and again after 6 months. According to the initial degree of neurological deficit, patients were stratified into a mild, intermediate and severe group (using a scoring system). After 2 weeks there was significantly less neurological deficit in the total glycerol-treated group than in the placebo group (2p less than 0.02). This favourable effect of glycerol was even greater in the patients with an initially intermediate degree of neurological deficity (2p less than 0.01). After 6 months there was no difference between the total glycerol-treated and the placebo group. A beneficial effect of glycerol treatment, however, was still demonstrable in the intermediate group (2p less than 0.05). Mortality was not influenced by glycerol treatment. No side effects of the glycerol treatment could be detected. Intravenous administration of 10% glycerol can thus be recommended in patients with acute cerebral infarction.
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From 1972 to 1974, the authors carried out logopaedic examinations of over 100 patients with retrodisplaced maxillae at the Clinic for Maxillo-Facial Surgery at the University of Zurich (Director: Prof. H. Obwegeser, M.D., D.M.D.). From this clinical material, 40 cases which were fully documented in respect of medical history, surgical treatment and speech behavior were selected, and the effect of the advancement of the maxilla on the individual ability to articulate was studied.
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The records of a total of 102 patients who underwent primary total hip replacement during 1987-88 were evaluated retrospectively. 36 patients had donated 1-3 units of whole blood preoperatively. Surgery was performed with the use of a device for intraoperative autotransfusion (IAT). Another 25 patients without preoperative autologous blood donation were operated with the use of IAT. None of these techniques was available for the remaining 41 patients. The mean perioperative blood loss and the mean volume of transfused blood were 1400 ml and 1000 ml respectively. Equal quantities of blood were lost intra- and postoperatively, whereas only one fifth of transfused blood was given intraoperatively. Homologous blood transfusion was not required in 32% of the patients for whom autologous blood was not available. However after preoperative autologous blood donation, 95% of the 2-unit donors and 100% of the 3-unit donors could be operated without homologous blood transfusion. Autologous blood donation did not increase the need for homologous blood transfusions. With the use of IAT it was only 20% of the patients that at least 500 ml of blood were salvaged for retransfusion. On the basis of these findings, elective primary total hip replacement would seem to be the ideal operation to be performed after preoperative autologous blood donation and, whenever possible with the use of IAT. The desirable ratio of 1,5:1 for the units of blood to be crossmatched preoperatively vs. units transfused perioperatively can be achieved solely by preoperative donation of 3 units of autologous blood.