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Biomedical subjects

I E Richter

Publications and source records attributed to I E Richter.

At least 19 recordsLinked to original sources

Effects of peptide hormones on urea- and glycogen-synthesis of isolated hepatocytes and the influence of a toxic factor from burnt mouse and human skin.

A toxic extent has been isolated and partially purified from burnt human and mouse skin and also from sera of severely burnt patients, which causes disturbances of energy metabolism and decreased synthesis rates for glucose and urea in the perfused rat liver. Enzymatically isolated hepatocytes from rat livers were used to study the toxic effects on hormonal sensitivity, synthetic functions and ultrastructure of the cells. A decreased synthesis of urea and glycogen was found in cells from rats treated 5 days before with "toxin" and in cells, which were directly incubated with the toxic factor. Glucagon increased urea synthesis in normal cells by 33%, and a decrease of 25% was caused by insulin. Cells of rats treated with the nontoxic precursor of the toxic factor from normal skin were similar, while those treated with "toxin" produced less urea and did not react to glucagon or insulin. Glycogen synthesis was reduced in cells directly incubated with the "toxin", however, the hormonal effects were still observed. Surface alterations of "toxin" treated cells and cells of "toxin" treated rats were found by scanning electronmicroscopy. These findings provide evidence of a direct cytotoxic effect of the toxic factor from burnt skin. It is proposed that the "toxin" acts on the cellular membrane with destruction of surface and receptorproteins.

Animals↗

[Therapy of toxin absorption in skin burns. Synthetic skin replacement or tannic acid (author's transl)].

The influence of toxic factors from burned skin on pathogenesis of burn disease has been demonstrated in recent years. For preparation for skin transplantation synthetic material is used. The present study was undertaken to investigate if such material could inhibit the resorption of toxic factors. Specific mitochondrial alterations, which are reproducibly found 5 days after skin burn or application of burn toxin, served as parameter. Rats, which were treated shortly after burn or later with tannic acid were used as controls. Glucose and urea were measured in serum to check the synthetic function. Therapy with Epigard resulted in a better general condition and normal values of glucose and urea, but no reduction of specific mitochondrial alterations. Treatment with tannic acid caused no improvement in general condition, glucose and urea levels were not significantly altered. Only the early application resulted in a reduction of mitochondrial alterations. An otherwise indicated therapy with a synthetic skin material is not suitable for inhibition of the resorption of toxic factors from burnt skin.

Animals↗

[Isolated liver cells of the rat under the influence of a toxic factor from burnt human and animal skin (author's transl)].

The existence of a burn toxin which could be responsible for the late burn disease has become increasingly accepted. The present study investigates both metabolism and ultrastructure of isolated rat hepatocytes both under the influence of a burn toxin isolated from burnt mouse and human skin and of its native nontoxic precursor. Cells from rats treated with toxin systematically were also investigated. The cells directly incubated with toxin showed no alterations of gluconeogenesis, but a reduced urea--and glycogensynthesis from most precursors used. Cells of pretreated rats were reduced in all functions and showed more distinct ultrastructural damage, while those incubated directly were significantly more altered. The results prove a direct toxic effect of a burn toxin on isolated liver cells.

Amino Acids↗

Effect of cutaneous human or mouse burn toxin on the metabolic function of isolated liver cells.

Studies on isolated perfused rat livers 5 days after either a sublethal burn or an i.p. injection of human/mouse burn toxin showed a significant inhibition of the glucose/urea synthesis and the ATP production concomitantly with ultrastructural mitochondrial damages. A direct specific effect of these burn toxins on enzymatically isolated liver parenchyma cells was found either after direct incubation of the isolated cells with the compound or 5 days after injection of the toxin to the animals followed by the isolation of the cells. Control experiments were performed with the "native" non-toxic precursor from normal skin. Liver cells of rats pretreated with the toxin showed an 100% increase of the amino-acid release while this increase was 70% after direct toxin incubation. Glycogen synthesis from lactate, alanin and fructose was significantly decreased in both toxin groups while the glucose synthesis was not altered. The degree of the inhibition of the glycogen synthesis was directly correlated to the number of ATP-dependent metabolic steps. A disturbance of the oxygen transfer system by structural damages of the mitochondria seems to be the basic mechanism for these specific metabolic alterations due to ultrastructural mitochondrial damages.

Adenosine Triphosphate↗

[Observations of the surface of the articular cartilage after treatment with hyaluronidase (author's transl)].

1. The articular surfaces of the femoral head of rats have been studied by scanning electron microscopy after in vitro treatment with hyaluronidase. 2. The cartilage surface has been digested mildly by the buffer medium (control). 3. The matrix of the cartilage has selectively been removed by the hyaluronidase. 4. Chondrocytes have been seen on the surface after treatment with hyaluronidase for a longer period. 5. We discuss the result of enzymatic digestion.

Animals↗

[The pros and cons of haemoperfusion (author's transl)].

6 patients with severe self-poisoning were treated by charcoal-haemoperfusion in our centre up to now. In four of them (all suffering from sleeping drug overdosage) the treatment was successful. Two patients with intoxications by agrochemicals died in spite of haemoperfusion. Side effects of haemoperfusion were drops of blood pressure and platelet count, depletion of immune bodies, and adsorption of remedies. Up to now, the indication for haemoperfusion has to consider these secondary actions of encapsulated charcoal as inevitable.

Arteries↗

Time sequence and site of fluid accumulation in experimental neurogenic pulmonary edema.

The initial phase of pulmonary edema development following intracranial pressure elevation was studied by means of transmission electron microscopy. Using perfusion fixation and application of a blood tracer (HRP horseradish peroxidase) the time sequence and site of fluid leakage out of pulmonary vessels was demonstrated: - passage of edema fluid through intercellular clefts of alveolar capillary endothelium - edema accumulation in alveolar interstitial tissue - draining of edema fluid from the alveolar septum to the interstitium of terminal bronchioli and to lymphatic vessels. An early interepithelial fluid leakage out of the alveolar wall remains questionable.

Animals↗

[The fine structure of liver sinusoids after perfusion fixation with various pressures. A transmission and scanning electron microscopic study (author's transl)].

The fixation of rat liver by perfusion with glutaraldehyde with different pressures has been investigated. For this study adult male albino rats were used. Rat livers were fixed by perfusion through the abdominal aorta according to the method of FORSSMANN et al. (1967). Perfusion pressures varied from 30 to 210 mmHg. A continuous complete endothelial lining of liver sinusoids could be visualized with TEM and SEM after fixation with perfusion pressures lower than 100 mmHg. Three different regions could be noticed in the endothelial cell: 1. prominent nucleous region, 2. compact cytoplasmic processions containing mitochondria and ergastoplasma, 3. delicate fenestrated cytoplasmic areals. As a rule the fenestrations were localized in groups, s.c. sieve plates. After perfusion fixation with pressures above 100 mmHg the endothelial lining of liver sinusoids appeared similar to a wide-meshed net. The sieve plates were destroyed, and numerous defects could be found in the endothelial cells. Hepatocytes showed vacuoles which seem to be due to invagination of the cellular membrane. For the development of artifacts even with physiological perfusion pressures in the aorta (110 mmHg), the content of procaine in the rinsing solution is responsible. Eliminating the function of arteriols leads to unphysiological pressure effects in the sinusoids.

Animals↗

[On the influence of hypoxia on the sinus endothelial cells of rat liver. A scanning and transmission electron microscopic investigation (author's transl)].

Fine structural alterations of liver sinusoids in young and adult albino rats breathing 6% oxygen in nitrogen at normal atmospheric pressure for periods from 3 to 30 h were described by use of TEM and SEM. After short-term hypoxia the fenestrated areas of endothelial cells were partially destroyed. After long--term hypoxia wide gaps could be visualized in the endothelium, too. In the liver specimens of all hypoxic animals electron lucent membrane bounded blebs arose from the endothelial lining. Cytoplasmic protrusions of hepatocytes bulged into the sinusoidal lumen. In the space of Disse and the sinusoidal lumen bleblike corpuscles and parts of cytoplasmic membrane being discharged from liver cell vacuoles could be observed. The find structure of liver sinusoids in hypoxia was very similar in young and adult albino rats. The findings suggest a discharge of metabolites and cellular components from endothelial cells and hepatocytes in a state of energetic insufficiency by forming cellular blebs and protrusions. It was supposed, that the combined effects of hypoxia and shearing of circulating blood were responsible for the development of holes and gaps in the endothelial lining.

Animals↗

[The structure of meningeal granules based on light- and scanning electron microscopic studies].

The granula meningica of man (medium and advanced age) were investigated by means of light microscopy and scanning electron microscopy. We established the following: 1. The endothel of the sinus durae matris of man only seldom shows the blind tubes of endothel which were described by Andres (1967)1 after investigations made in cats and dogs. 2. a) There are no tube systems lined with mesothelial cells in the tissue of the granula meningica. Usually the cellcords and cellclusters are solid. Only in exceptional cases do they have a cavity. b) There are wide spaces between the collagen fibrebundles. These spaces are filled with a thinly liquid amorphous ground substance. We observed many free cells there (especially macrophages). 3. The construction of the connective tissue of the granula meningea lead us to conclude, that they are capable of changing their volume and shape considerably. The possible functional consequences of these results were discussed.

Aged↗