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.
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.
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