Search Results - (Author, Cooperation:P. Weissgerber)

2011-11-05

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Iris/anatomy & histology/cytology/*metabolism/*radiation effects ; Light Signal Transduction/physiology/*radiation effects ; Mammals/*physiology ; Mice ; Phospholipase C beta/metabolism ; Photic Stimulation ; Primates/physiology ; Reflex, Pupillary/physiology/radiation effects ; Retina/cytology/*metabolism/*radiation effects ; Retinal Ganglion Cells/metabolism/radiation effects ; Rod Opsins/*metabolism

1433-8580

Somatostatin ; Cancer cell stickiness ; Platelet adhesion and aggregation in vivo

Springer Online Journal Archives 1860-2000

Medicine

Summary We employed a test model, which we had developed for the investigation of platelet adhesiveness and aggregation in vivo. Our experiments demonstrated that somatostatin is not only able to dose-dependently inhibit the stickiness of i.v. injected Walker 256 carcinosarcoma cells to the vascular endothelium of the rat mesentery and the drastic, immediate reduction of platelet count in venous blood, but also to significantly reduce the rate of instantly occurring terminal tumor cell embolism of the lung. These actions may be explained as being mediated via an inhibition of platelet adhesion and aggregation to circulating cancer cells. Because some oral antidiabetics showed a similar but weaker effect in our test system (Gastpar et al. 1982), it should be examined as to whether the in vivo inhibition of platelet adhesiveness and aggregation of the investigated compounds are mediated by a somatostatin release from the pancreas.

Electronic Resource

1433-8580

Cancer cell stickiness ; Platelet adhesion and aggregation in vivo ; Oral antidiabetics

Springer Online Journal Archives 1860-2000

Medicine

Summary Employing the test model which we developed for the investigation of platelet adhesiveness and aggregation in vivo, experiments demonstrated that the sulfonyl urea derivatives, glibenclamide, gliclazide, and HB 180, as well as the carboxylic acid derivative, meglitinide, are able to inhibit, in a dosedependent relationship, the adherence of i.v. injected Walker-256-carcinosarcoma cells to the vascular endothelium of the rat mesentery, as well as to reduce significantly the rate of instantly occurring terminal tumor cell embolism of the lung. Since venous blood platelet count in surviving animals is inversely proportional to the number of the tumor cells which adhere to the vascular endothelium, one can deduce that tumor cell embolism is an immediate result of a massively occurring disseminated intravascular coagulation (DIC) which may be induced by i.v. injection of thromboplastic active carcinosarcoma cells and leads primarily to a drastic platelet count reduction. All four substances inhibit this platelet count reduction as well as the directly correlated tumor cell embolism mortality rate in a linear dose-dependent fashion. Their action can therefore be explained as being mediated via an inhibition of platelet adhesion and aggregation to the circulating tumor cells. Our proof of platelet aggregation in vivo correlates with the results obtained by Klaff et al. (1979), as far as a normalization of the pathologically increased platelet aggregation tendency in vitro in diabetics following 4–6 weeks of therapy with the sulfonyl urea derivatives glibenclamide and gliclazide.

Electronic Resource