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Biomedical subjects

C Mittermayer

Publications and source records attributed to C Mittermayer.

At least 127 records · Page 7Linked to original sources
PubMed1984

Volume elasticity, modulus of elasticity and compliance of normal and arteriosclerotic human aorta.

In order to measure the flow-dynamical effect of arteriosclerotic changes of the vessel wall we determined volume elasticity E' and modulus of elasticity of 53 human aortae in a static p-V-test as other authors did, too. The p-V-curves are normalized to the aortic basic volume Vo, so that we could determine the haemodynamic effect of arteriosclerosis immediately from E' and. Diameter, length, and, accordingly, the basic volume of the aorta without prestressing increase significantly in aortae with severe arteriosclerosis in comparison to those without sclerosis. The volume elasticity E' as a function of the static aortic pressure has a minimum within physiological pressure range and changes into a linear function when arteriosclerosis increases. The modulus of elasticity of a normal aorta remains constant within a pressure range of 20 to 100 mm Hg and it shows a linear increase at higher pressure. The differences between Vo, E' and of aortae with and without severe arteriosclerosis, however, are highly significant.

Adult↗
PubMed1982

Proliferative response of human endothelial cultures to various types and treatments of human sera, to culture treatments and to various oxygen concentrations.

Endothelial cells from the human umbilical vein were exposed to different human sera, differently treated serum, to various oxygen concentrations, and various culture treatments. Endothelial proliferation was determined by measuring the uptake of [3H]-thymidine by means of autoradiography and presented as thymidine labeling index (TI) values. TI values differed according to different serum concentrations, serum types, serum preparations (WBS-PDS) and serum pretreatments. Low oxygen concentrations in the incubator atmosphere induced an early DNA synthesis response without an increase in cell number. The addition of the protease inhibitors aprotinin and soybean trypsin inhibitor to the culture medium resulted in a dose dependent TI decrease, whereas PMSF showed no influence.

Blood↗
PubMed1982

Human endothelial cell proliferation inhibiting activity in the sera of patients suffering from 'shock' or 'sepsis'.

The response of DNA-synthesis of human endothelial cells to sera derived from twenty-five patients suffering from 'sepsis' or 'shock' was measured by autoradiographic methods. In eight cases a constant decrease in proliferative response was found compared to that of sera from healthy donors. These proliferation values were shown to lie below the '60%-of-control-line'. The difference between the means of control and of corresponding 'low-response' values was significant (P less than 0.05). In three cases a diminished response was caused only by some of several serum samples taken at different times. These results correlated well with the clinical state and outcome of patients but not with any of the over sixty clinical, therapeutic, laboratory and post-mortem parameters of investigation. Evidence is presented for a proliferation inhibiting activity in sera of patients in clinically poor states, and some physico-chemical properties of this 'factor' are described. Lethal injury to the cells or an impairment of cellular migration could not be observed within the observation periods used in this study.

Cell Division↗
PubMed1982

The proliferation-inhibiting effect of endotoxin on human endothelial cells in culture and its possible implication in states of shock.

The aim of this study was to determine whether bacterial endotoxin (LPS) could be responsible for the in vitro endothelial proliferation-inhibiting activity found in some serum samples derived from patients suffering from "sepsis" or "shock." DNA-synthesis response of cultured human endothelial cells was measured by autoradiographic methods. We found a dose-dependent decrease in the proliferation-inducing capacity of human serum after the addition of endotoxin without any detectable cellular injury. This effect depended on the serum concentration in the culture medium: higher serum concentrations reduced the measurable LPS-activity. The endotoxin effect turned out to be preventable when LPS sera were preincubated with different concentrations of Polymyxin B sulphate. That treatment also seemed to prevent the inhibiting effect of some patient sera. The inhibiting effect of both the LPS-serum and the patient serum could be reversed by washing and adding fresh human serum. We conclude that the endothelial regeneration-inhibiting activity of endotoxin may play an important role in the irreversibility of certain shock states.

Autoradiography↗
PubMed1981

[Pathology and pathophysiology of circulatory shock with respect to shock lung (author's transl)].

The circulatory and acute generalized failure of the circulation, in particular of the lesser peripheral circulation, and may possibly but not necessarily be accompanied by a decrease in blood pressure and damage to the tissue due to a lack of oxygen. The main question concerning the causal pathogenesis of shock is still unsettled, but an interaction between a lack of oxygen as well as of other factors, like endotoxin, complements and vasoactive amines, and the presence of a microthrombosis must be held responsible for the appearance of this condition. In modern intensive medicine the lung must be considered as the preferential area for the manifestation of shock. The clinical picture of shock lung may be described as acute respiratory deficiency accompanied by an impaired diffusion of oxygen, an increase in dead-space ventilation together with an increased shunt volume and intensified respiratory activity. The pathology of shock lung shows two phases and has its onset in exudative alveolitis followed by alveolar fibrosis which can be hardly be controlled by therapy. The early phase of shock lung manifesting itself by exudative alveolitis is decisive with regard to diagnosis and further therapeutic measurements. If the condition can be brought under control at this stage there is a chance that the patient may survive.

Disseminated Intravascular Coagulation↗
PubMed1981

Urethane-induced lung hyperplasia: carboxylesterase isozymes as markers in lung pathology.

Following a 3- to 5-week exposure to urethane (0.1 per cent in drinking water) a 2-fold increase of total esterase activity per lung was observed. The specific activity of lung esterase was raised from 23 to 31 units per gm. wet weight. Concomitantly, the number of esterase-positive cells (predominately type II alveolar lining cells (pneumocytes and macrophages) increased. As a consequence of urethane treatment, abundant esterase-rich lamellar bodies looked as if they had just been extruded into the alveolar space. This reaction suggests that, even in pathologic states, esterase activity is associated with lamellar bodies. Electrophoretically, esterase-1 was increased and the pattern of esterase-7 was changed, whereas the other isozymes of carboxylesterase did not differ from the control. The hypothesis is made that multilamellar bodies are the subcellular sites of esterase-7 and that macrophages are the location of esterase-1. Since distinct carboxylesterase isozymes seem to be specifically associated with different subcellular structures of the lung and their activity increases in lung hyperplasia, they may be useful marker enzymes for physiologic and pathologic events in lung function.

Animals↗