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Biomedical subjects

J Staubesand

Publications and source records attributed to J Staubesand.

At least 37 records · Page 2Linked to original sources
PubMed1981

Isolation, identification, and continuous culture of coronary endothelial cells from guinea pig hearts.

Viable and homogeneous endothelial cells were obtained from isolated guinea pig hearts by application of a special perfusion technique of the coronary system with an isotonic collagenase-trypsin solution and subsequent purification of the dissociated cells by Percoll density gradient centrifugation. The coronary endothelial cells were grown in tissue culture for periods up to 7 months. Serial passage proved to be possible. During logarithmic growth, generation time was found to be 18 h; it could be reduced to 16 h by addition of thrombin to the culture medium. Light, phase contrast and scanning electron microscopy as well as autoradiography revealed that cultured coronary endothelial cells grew as strict monolayers of closely apposed, polygonal large cells. By scanning electron microscopy, it could be demonstrated that the morphology of the cultured cells changes characteristically during attachment of the cells to their substratum. The changes observed were very similar to those of proliferating endothelial cells of isolated coronary vessels kept in organ culture. According to transmission electron microscopy studies, cultured coronary endothelial cells proved to contain only an extremely small number of Weibel-Palade bodies. Nucleoside phosphorylase (EC 2.4.2.5.) and 5'-nucleotidase (EC 3.1.3.5.) were identified in freshly isolated as well as in cultured endothelial cells. Their specific and total activities proved to be much higher than in myocardial tissue, thus indicating a prominent role of nucleotide metabolism in the coronary endothelium.

Animals↗
PubMed1981

[Electron microscopic and cytochemical data on the interaction between endothelial cells and thrombocytes].

The data obtained demonstrate that besides the known adhesion and aggregation of thrombocytes when intima is injured and endothelium is desquamated, there are some other mechanisms. Thus, the thrombocytic aggregation is possible in the area of intracellular accumulation of lipid inclusions and calcium depositions in the uninjured endothelial cells. A suggestion is made on a trigger role of the external membrane of the endotheliocyte in this process.

Animals↗
PubMed1980

Early micro- and macro-angiopathy in the streptozotocin diabetic minipig.

Streptozotocin diabetes in the minipig constitutes an outstanding model for the study of diabetic angiopathies. Changes which are classified as macroangiopathy are evident after 6 months, while the first changes indicative of microangiopathy appear already after about 18 months. The degree of pronouncement of the microangiopathy depends on the duration and severity of the induced diabetes. These results constitute a cogent argument in favour of the "metabolic theory" of the development of diabetic microangiopathy.

Animals↗
PubMed1980

An investigation into the fine structure of the ligated rat ureter.

The normal structure of the ureter of the rat is described and compared with the results of earlier work. Research on arteries left in situ stimulated morphological investigation of the ligated ureter proximally and distally to the ligature. As in ligated blood vessels, an increase in modified muscle cells with accompanying increase in connective tissue (particularly proximally to the ligature) occurs in the ureter. In association with quantitative changes, qualitative changes in the formation of collagen and in the arrangement of fibrils were found, although not so marked as in arteries subjected to "load failure". During a comparison of the ureteric walls on either side of a ligature intracellular collagen was found. The results of earlier work on ligated ureters are discussed, together with the present findings. The reactions of ureteric and arterial walls subjected to similar "load failures" are compared. Qualitative changes in the intercellular substance are considered in connection with the findings in cases of pathological processes in the walls of blood vessels. Several possibilities are suggested with regard to the interpretation of the intracellular collagen.

Animals↗
PubMed1980

The ultrastructural characteristics of abnormal collagen fibrils in various organs.

Quite unrelated diseases affecting different organs can lead to the appearance of abnormal collagen fibrils, which may be due to genetic disorders, transformation of mesenchyme cells, increased collagen synthesis or a change in the ground-substance. The simultaneous appearance of abnormal collagen fibrils and matrix vesicles containing lysosomal enzymes in the majority of our electron photomicrographs suggests an alteration in the ground-substance as a main cause of non-hereditary collagen dysplasia.

Animals↗
PubMed1980

Ultrastructural and morphometric investigations into the arterial wall of the genetically hypertensive rat.

A number of injurious agents, including "load-failure" of hemodynamic or metabolic origin, constitute "risk factors"for the wall of a blood vessel. We are here concerned with arterial hypertension, which is a primary risk factor for the production of atherosclerotic change. The SHR (spontaneously hypertensive rat) has been included among the more extensive series of experiments conducted by our research team (STAUBESAND et al.) as a particular model for the investigation of metabolic and hemodynamic "load-failure". The aims of the present contribution are to describe the morphological changes in the diseased vessel wall and to support these findings morphometrically.

Aging↗
PubMed1979

[A new concept of the pathogenesis of medial dysplasia (author's transl)].

A unifying concept may be set out briefly in the following manner: injurious agents (such as abnormal hemodynamic and/or metabolic conditions--"risk factors for the vessel wall") leads to the transformation of contractile (k) smooth muscle cells into the metabolically more active or "modified" (m) variety leads to an increase in the number of intracellular and extracellular lysosomes (matrix lysosomes) leads to medial dysplasia. The vague concept of a "vessel wall weakness" as the cause of aneurysms, varicose veins etc. has given place to a more precise picture, following the E. M. demonstration of atypical (i.e. dysplastic) collagen fibrils and elastic fibres. The muscle cells of the vessel wall appear to react to the altered conditions with an icrease of lysosomes, and therefore of lysosomal enzymes. The E. M. has also revealed collagenolysis, elastolysis and proteoglycanolysis in the vicinity of matrix lysosomes.

Animals↗
PubMed1979

Collagen dysplasia and matrix vesicles. Researches with the electron microscope into the problem of so-called "weakness of the vessel wall".

Quite diverse pathological changes of the wall of a blood-vessel can lead to quantitatively and qualitatively altered collagen, as well as to the production of matrix vesicles. It can be demonstrated morphologically that changes--particularly qualitative changes--in collagen are accompanied by a more or less severe loss of function. Possible causal connections between the appearance simultaneously of matrix vesicles (in which lysosomal enzymes can be demonstrated) and altered vascular collagen are discussed.

Aged↗