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I Winter

Publications and source records attributed to I Winter.

35 records · Page 2Linked to original sources

Fendiline and calmidazolium enhance the release of endothelium-derived relaxant factor and of prostacyclin from cultured endothelial cells.

We investigated the effects of fendiline, calmidazolium and trifluoperazine, compounds described as calmodulin antagonists, on the release of the endothelial autacoids prostacyclin (PGI2) and endothelium-derived relaxant factor (EDRF). Cultured bovine aortic endothelial cells were grown on microcarrier beads and continuously superfused with Tyrode's solution. Samples collected from the superfusate were assayed for PGI2 concentration (6-keto PGF1 alpha radioimmunoassay) and for EDRF activity (stimulation of soluble guanylate cyclase in vitro). Stimulation of endothelial cells by ATP (3 microM) resulted in a 6.9 +/- 1.4-fold increase of PGI2 concentration in the superfusate (p less than 0.01) and an 8.6 +/- 3.4-fold enhanced guanylate cyclase activity (p less than 0.01). In the presence of calmidazolium (10 microM), the basal values of PGI2 concentration increased 28-fold (p less than 0.01) and the guanylate cyclase activity 10-fold (p less than 0.01). Further enhancement of both was observed after additional administration of ATP. Fendiline (30 microM) did not affect autacoid release by non-stimulated cells. However, the ATP-induced release of PGI2 and EDRF was more than doubled (p less than 0.01) in the presence of this drug compared to ATP-stimulation alone. Trifluoperazine (10 microM) had no enhancing effect on EDRF release, and the ATP-induced release of PGI2 was even significantly attenuated by 84 +/- 12% (p less than 0.01). Calmidazolium and fendiline were also applied to endothelial cells loaded with the fluorescent indicator of free calcium concentration (Ca2i+), indo-1. However, effects of calmidazolium on Ca2i+ could not be quantified since calmidazolium caused some leakage of indo-1 out of the cells. A smaller leakage was observed during the combined application of fendiline and ATP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Characterization of vascular relaxant factor released from cultured endothelial cells.

Cultured bovine endothelial cells were grown on microcarrier beads. Columns (0.2 ml) packed with microcarriers were perfused with oxygenated (20% O2) Tyrode's solution containing indomethacin (10 microM), and the effluent was passed through precontracted, endothelium-denuded detector arteries. When the endothelial cells were stimulated with bradykinin (3-100 nM), adenosine 5'-triphosphate (0.3-30 microM), or calcium ionophore A23187 (10-300 nM), they released dose-dependently a nonprostanoid compound that dilated the detector vessel. The factor, probably identical to the endothelium-derived relaxing factor of native endothelium, evoked dilations of the same magnitude in different types of detector vessels (rabbit thoracic aorta, rabbit femoral artery, canine coronary artery). However, this relaxant factor was significantly more effective in arteries precontracted by norepinephrine or serotonin than in arteries precontracted by potassium depolarization. Thus, its dilator action resembles that of the nitrovasodilators. The factor is labile, with an apparent half-life in the range of 20 to 30 seconds. Its dilator potency was inhibited by dithiothreitol (0.2 mM), metyrapone (0.2 mM), nordihydroguaiaretic acid (20 microM), and hemoglobin (1 microM), all of which apparently inactivated the factor. Synthesis or release (or both) of the relaxant factor was abolished by methylene blue (1 microM). High PO2 levels (greater than 400 mm Hg) in the perfusate markedly reduced the release of the relaxant factor from the cultured cells. This study demonstrates that a vascular relaxant factor is released from endothelial cells in monoculture by adenosine 5'-triphosphate, bradykinin, and A23187 and establishes such a culture as a useful tool for analyzing the mechanisms of endothelium-dependent vasomotion.

Adenosine Triphosphate↗

1a,25-Dihydroxyvitamin D3 stimulates alkaline phosphatase activity and inhibits soft-tissue proliferation in implants of bone matrix.

To test the importance of vitamin D metabolites on intramuscular implants of demineralized bone, four-month-old rats were given either 1a,25-(OH)2D3 or 24R,25-(OH)2D3, or a combination of both metabolites, and sacrificed at intervals ranging from five to 35 days after implantation. Histologically there was a reduced ingrowth of mesenchymal cells into the implanted matrix cylinders in the presence of 1a,25-(OH)2D3; the reduction was followed by decreased total DNA and protein values until the 16th experimental day. At 35 days postimplantation, the quantity of new bone was the same in all treated groups. However, 1a,25-(OH)2D3 increased the alkaline phosphatase activity 60%-110% (depending on the denominator used). The metabolite 24R,25-(OH)2R3 had no effect on cell growth or the alkaline phosphatase activity. These results provide evidence for the inhibitory effect of 1a,25-(OH)2D3 on mesenchymal cell growth and its stimulatory effect on osteoblasts, which are responsible for increased alkaline phosphatase activity and new bone formation in vivo.

24,25-Dihydroxyvitamin D 3↗

[The problem of osteosynthesis in peripheral replantation].

In this report, 16 cases of peripheral replantation are described, in which osteosynthesis was carried out by means of AO-mini or small-fragment plates with the obvious advantage of allowing early mobilisation. A disadvantage of this method is that it is necessary to dissect the soft tissue to a greater extent and to elevate the periosteum more than in using Kirschner wires, this dissection to permit sufficient fixation of the plate and screws. As a result, primary technical difficulties in the venous anastomosis may occur and there is a risk of adhesions developing between the extensor apparatus and the bone (two cases). Difficulties occur when using plates and screws for comminuted and juxtaarticular fractures. In these cases Kirschner wire osteosynthesis is preferred. For injuries in zones 1 and 2 in the majority of the cases an osteosynthesis with wire is indicated. Only in cases of replantation in zone 2, where the DIP joint is destroyed, can an arthrodesis be performed by means of a screw. When using the above mentioned osteosynthesis for peripheral replantations, we have achieved good to very good end results in the majority of the cases.

Amputation, Traumatic↗

[Not Available].

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Germany↗

[Not Available].

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Germany↗

[Not Available].

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Economics, Medical↗