Biomedical subjects

A G Grøthe

Publications and source records attributed to A G Grøthe.

4 recordsLinked to original sources

PubMed1988

Sequence of cellular responses in rabbit aortas following one and two injuries with a balloon catheter.

In order to further elucidate the pathogenesis of intimal proliferation and increased thrombogenesis following repeated arterial injuries we studied the sequence of the cellular changes following two injuries of rabbit aortas with a balloon catheter. Following the first injury, the de-endothelialized surface was covered by a platelet monolayer. Polymorphonuclear leucocytes adhered to the inner surface of this monolayer and did not appear to penetrate the vessel wall. By 4 to 7 days, areas of neointima had formed. Within seconds after the reinjury at 7 days after the de-endothelialization small platelet aggregates formed on injured neointimal smooth muscle cells. Within I min platelet thrombi and fibrin strands formed. At 30 min most of the platelet thrombi had become fibrin-rich. Polymorphonuclear leucocytes had accumulated and many had begun to penetrate into the neointimal tissue. The number and extent of penetration of leucocytes into the inner parts of the arterial wall increased with time. Four days after the injury the neointimal cushions were restored and thickened. Both following the first and second injury the formation of neointimal cushions was accompanied by a change in the polarity of the inner layers of medial smooth muscle cells, some of which appeared to have migrated into the neointima.

Animals↗

PubMed1988

Distribution of cellular responses in rabbit aortae following one and two injuries with a balloon catheter.

To investigate the mechanisms involved in the cellular reactions to arterial injuries, we studied the distribution of the deposits on the injured intima and the pattern of neointimal thickening following single and double injuries of rabbit aortae with a balloon catheter. Thirty minutes after the first injury most, but not all, of the inner surface of the aortae was covered by adherent, spread platelets. Seven days following the first injury areas of neointima, mainly proliferating smooth muscle cells, had formed around and opposite the orifices of branch vessels. The rest of the inner aortic surface consisted of acellular subendothelial matrix. Thirty minutes after the second injury, 7 days after the first, single platelets adhered once more to parts of the reinjured subendothelium, mostly between the orifices. Numerous fibrin-rich, platelet thrombi were present mainly on the surface of the injured neointima. Thirty minutes after both the first and second injury polymorphonuclear leucocytes adhered to the inner surface downstream from the orifices of branch vessels and in longitudinally oriented zones opposite the orifices. Four days following the second injury, the neointima was restored with the same distribution as before the second injury, and few thrombi, adherent platelets, or leucocytes remained.

Animals↗

PubMed1986

Injury to cultured endothelial cells by thrombin-stimulated platelets.

In vivo, stimulated platelets may injure the endothelium. We have used cultured endothelial cells to assess endothelial cell damage caused by platelet stimulation with thrombin. Endothelial cells were cultured from umbilical veins and semiconfluent cultures were labeled with Na2 51CrO4. Twenty four hours later washed human platelets (final concentration 200,000 platelets/microliters) and thrombin (final concentration 4 units/ml) were added to the medium and the culture dish was shaken for 15 minutes. The percentage of cells detached from the culture dish and the percentage of 51Cr lost from the endothelial cells into the ambient fluid during the shaking were determined and used as indicators of cell injury. Increased percentages of loosened cells and 51Cr in the ambient fluid were observed with platelet suspension and thrombin compared to controls with neither platelet suspension nor thrombin and controls with either platelet suspension or thrombin. The platelet-free supernatant obtained after reaction of the platelets with thrombin also increased the percentage of loosened cells, but it did not increase the percentage of 51Cr in the ambient fluid to a significant degree. Thrombin alone caused a moderate loss of 51Cr, but no increased loosening of cells. Treatment of the platelets with acetylsalicylic acid prior to the experiment depressed the detachment effect of thrombin-stimulated platelets, but did not alter the effect on the release of 51Cr into the ambient fluid. Scanning and transmission electron microscopy of cultured endothelial cells exposed to thrombin-stimulated platelets confirmed the presence of loosening and injury to the endothelial cells. Thus, platelet stimulation with thrombin had at least two effects on the cultured endothelial cells: a loosening effect caused by material released from the platelets; an injury effect which, in order to reach its maximum, required the presence of stimulated platelets.

Aspirin↗

PubMed1984

A simple device for staining electron microscopy grids.

A simple holder for electron microscopy grids is described. It consists of a rod covered with dental wax (Ladd, Cat. No. 32165). Multiple slits for holding grids are made in the wax. The rod is attached to a rubber cork that fits into the test tubes filled with staining or rinsing solutions. The device has simplified and standardized the staining procedure, and stain precipitates due to air exposure are avoided.

Microscopy, Electron↗