Ultrastructural changes in the rat liver during Euro-Collins storage, compared with hypothermic in vitro ischemia

Myagkaya, G.; Veen, Henk A. van; James, J.

doi:10.1007/bf02890241

Cited by 33 publications

(10 citation statements)

References 18 publications

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“…Blebs may be shed [19,23] and cause circulatory disturbance [28]; large blebs may narrow sinusoidal lumina and cause death after transplantation. Blebs formed following hypothermic liver preservation {26, 27,29], or hypoxia [22,23] are considered to originate from hepatocytes. In our study, there were two kinds of blebs, small (0.05-0.2 mm) and large (several mm).…”

Section: Discussionmentioning

confidence: 99%

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Ultrastructural changes in hepatocytes, sinusoidal endothelial cells and macrophages in hypothermic preservation of the rat liver with University of Wisconsin solution

Okouchi

Sasaki

Tamaki

1994

Vichows Archiv A Pathol Anat

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To identify subtle changes which might lead to liver failure after liver transplantation, rat livers stored at 4 degrees C in University of Wisconsin solution for 8, 16, 24, and 32 h were examined by transmission electron microscopy, scanning electron microscopy, cellular matrix maceration and freeze fracture for ultrastructural analysis. Endothelial cells exhibited aggregation of intramembrane particles (IMPs) at 8 h and produced tiny blebs accompanied by marked development of pits. As deterioration advanced, endothelial cells exposed the perisinusoidal faces of hepatocytes directly to the lumen with destruction of sieve plates. They then degraded with loss of IMPs. Macrophages followed a similar deterioration process to endothelial cells. Membranes of hepatocytes did not demonstrate aggregations of IMPs for 32 h. Rough endoplasmic reticulum (rER) lost ribosomes and smooth ER (sER) increased in amount and dilated in an irregular form. Autophagosomes appeared in the cytoplasm, engulfed cytoplasmic matrix containing intracellular organelles and became autophagic vacuoles. At 32 h bile canaliculi were filled with detached vesicles. This may be one of the causes of preservation related bile duct complications after liver transplantation.

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Section: Discussionmentioning

confidence: 99%

“…Bleb formation is one of the major ultrastructural changes seen in the sinusoid of preserved liver, and occurs mainly in hepatocytes [26,28,29]. Why blebs are formed on ultrastructurally well maintained hepatocytes is unknown.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural changes in hepatocytes, sinusoidal endothelial cells and macrophages in hypothermic preservation of the rat liver with University of Wisconsin solution

Okouchi

Sasaki

Tamaki

1994

Vichows Archiv A Pathol Anat

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“…The results indicated that after more than 8 hr of cold ischemic storage, a selective injury occurred to nonparenchymal cells based on trypan blue labeling. Other investigators (6,7) have also recently noted nonparenchymal cell injury based on morphological changes. The latter workers concluded that cell killing occurred during the cold ischemic interval, whereas our data suggested that lethal injury was precipitated by reperfusion.…”

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confidence: 94%

Reperfusion injury to endothelial cells following cold ischemic storage of rat livers

et al. 1989

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Storage of donor livers in Euro-Collins solution for human transplantation surgery is limited to about 8 hr. Here, tissue damage to isolated rat livers stored under the same conditions as human livers was characterized following reperfusion. The purpose of this work was to determine the importance of nutritional status on injury due to cold storage and reperfusion, to establish whether lethal injury occurs during cold storage or only after reperfusion, and to identify the cell types most vulnerable to damage. Rat livers were perfused with Krebs-Henseleit-bicarbonate buffer, stored 8 to 48 hr in Euro-Collins solution and reperfused with warm, oxygenated Krebs-Henseleit buffer for 15 min. Nuclear trypan blue uptake and lactate dehydrogenase release were used as indices of cell death. After 8 hr of cold storage and reperfusion, little loss of parenchymal or nonparenchymal viability occurred. After 24 or 48 hr, virtually all parenchymal cells remained viable. However, severe damage to nonparenchymal cells was observed, and about 40% of nonparenchymal cells were trypan blue positive. Nutritional status (fed vs. fasted) did not affect the extent of cell damage. Nonparenchymal cell killing was accompanied by cellular rounding, nuclear pyknosis and protrusion of cells into sinusoidal lumens. Scanning electron micrographs demonstrated denudation of the sinusoidal lining. Rounding and pyknosis were not observed in 24-hr-stored livers which were not reperfused, and trypan blue uptake did not occur in stored livers infused with cold, anoxic Euro-Collins solution. Based on cytochemistry and electron microscopy, lethal cell injury occurred predominantly to endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…The authors suggested that liver parenchymal cells were damaged mainly during reflow, as the consequence of microcirculatory disturbances. Myagkaya et al (1987) have also shown that, after flushing rat livers at 17°C with Eurocollins and preserving small pieces of perfused liver in Eurocollins at 4°C, selective lesions of endothelial cells can occur. After 12 hr, interruptions in the continuity of the endothelial lining were regularly observed and the nuclear chromatin of these cells showed pronounced clumping.…”

Section: Hypothermic Preservationmentioning

confidence: 95%

Hepatic circulation: Potential for therapeutic intervention

Ballet

1990

Pharmacology & Therapeutics

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In recent years, knowledge of the physiology and pharmacology of hepatic circulation has grown rapidly. Liver microcirculation has a unique design that allows very efficient exchange processes between plasma and liver cells, even when severe constraints are imposed upon the system, i.e. in stressful situations. Furthermore, it has been recognized recently that sinusoids and their associated cells can no longer be considered only as passive structures ensuring the dispersion of molecules in the liver, but represent a very sophisticated network that protects and regulates parenchymal cells through a variety of mediators. Finally, vascular abnormalities are a prominent feature of a number of liver pathological processes, including cirrhosis and liver cell necrosis whether induced by alcohol, ischemia, endotoxins, virus or chemicals. Although it is not clear whether vascular lesions can be the primary events that lead to hepatocyte injury, the main interest of these findings is that liver microcirculation could represent a potential target for drug action in these conditions.

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Ultrastructural changes in the rat liver during Euro-Collins storage, compared with hypothermic in vitro ischemia

Cited by 33 publications

References 18 publications

Ultrastructural changes in hepatocytes, sinusoidal endothelial cells and macrophages in hypothermic preservation of the rat liver with University of Wisconsin solution

Ultrastructural changes in hepatocytes, sinusoidal endothelial cells and macrophages in hypothermic preservation of the rat liver with University of Wisconsin solution

Reperfusion injury to endothelial cells following cold ischemic storage of rat livers

Hepatic circulation: Potential for therapeutic intervention

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