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.

No abstract

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.

No abstract

No abstract

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.

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.

1. It is well known that microscopically small particles may be absorbed from the peritoneal cavity via the large lymphatic vessels. The present experiments were carried out in order to elucidate the site of the absorption. In addition, the role of transperitoneal transport of neoplastic cells as a possible cause of cancer metastases was studied. 2. The peritoneal surface of 40 rats and mice was studied with the scanning electron microscope (diaphragm, lateral abdominal wall). The investigations were carried out in 8 rats and 3 mice 24 hrs following the intraperitoneal injection of washed homologous erythrocytes and in 20 rats and 5 mice 24 hrs after the intraperitoneal injection of Ehrlich ascites tumor cells. 2 rats and 2 mice served as controls. 3. In the control animals no stomata could be shown in the peritoneum of the diaphragm or in the lateral abdominal wall. 4. The i.p. injection of erythrocytes was followed by the appearance of stomata in the peritoneal surface of the diaphragm, and absorption of erythrocytes could be demonstrated. No stomata were found in the peritoneum of the lateral abdominal wall. 5. Tumor cells were found in the stomata following the i.p. injection of ascites tumor cells. It is concluded that a lympho-hematogenous spread of tumor cells seems probable at least in the early stage of tumor infiltration of the peritoneum. This stage is followed by implantation of the tumor cells on the peritoneum.