Lipid Peroxidation and Ultrastructural Changes in Rat Lung Isografts After Single-Passage Organ Flush and 48-Hour Cold Storage With and Without One-Hour Reperfusion in Vivo

Ma, Pickford; Jd, Gower; Doré, C; Pr, Fryer; Green, CJ

doi:10.1097/00007890-199008000-00008

Cited by 26 publications

(12 citation statements)

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“…In view of the central role which redox-active iron complexes play in the generation of highly toxic free radical species, the possible ameliorative effects of DFX have been previously studied. This chelating agent has been shown to be effective at reducing oxidative membrane damage following ischaemic insults to rabbit kidneys 1,15, 16], rat lung [12] and skin flaps 1,25] and to improve significantly some aspects of reperfusion damage such as the loss of endothelial cells in the lung 1,12] and smooth muscle cells in skin flaps 1,25]. However, in our laboratory, this decrease in lipid peroxidation was not accompanied by a concomitant increase in the survival of any of these tissues upon transplantation when DFX was administered alone [25,26].…”

Section: Discussionmentioning

confidence: 99%

“…There are some reports that DFX reduces ischaemia/reperfusion injury to the heart [9] although the addition of DFX to the St. Thomas' Hospital cardioplegic solution had no ameliorative effect on transplanted rat hearts which had been stored for 10 h at 0-4~ [10]. DFX has also been reported to improve preservation of canine lungs stored hypothermically in Euro-Collins solution for 24 h [11] and to prevent endothelial cell loss during the storage of rat lungs [12], although no overall improvement in viability was apparent in the latter model. Perfusion of canine kidneys with DFX after cold-storage in Euro-Collins solution for 24-48 h had no effect on subsequent viability of the organs assessed on an isolated perfusion apparatus [13].…”

Section: Introductionmentioning

confidence: 99%

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The effect of a synthetic hexadentate iron chelator (CP130) and desferrioxamine on rabbit kidneys exposed to cold and warm ischaemia

et al. 1993

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The effect of CP130 (a synthetic hexadentate pyridinone iron chelator) on the formation of two markers of lipid peroxidation (TBA-reactive material and Schiff's bases) in rabbit kidneys following a 72 h period of cold (0-4 degrees C) ischaemia was investigated by either adding CP130 to the flush/storage solution (hypertonic citrate solution) or by administering the agent intravenously 15 min before removal of the organs. In both cases, CP130 blocked the adverse rises in lipid peroxidation caused by ischaemia and subsequent reoxygenation of the homogenates in vitro. Both CP130 and desferrioxamine (DFX) (administered intravenously 15 min before ischaemia and 5 min before reperfusion) were also found to significantly reduce post-ischaemic rates of in vitro lipid peroxidation in kidneys rendered warm ischaemic for 90 min followed by reperfusion for 5 or 60 min in situ. Kidneys exposed to warm ischaemia and reperfusion developed interstitial and intracellular oedema, congestion and haemorrhage. DFX administration had little effect on the histological outcome, whereas CP130 significantly reduced interstitial oedema (at 5 min reperfusion compared to the DFX-treated group), intracellular oedema (at 60 min reperfusion compared to the DFX-treated group) and congestion (at 5 min reperfusion compared with a control group not given any agent). It is concluded that while CP130 and DFX exhibited similar antioxidant properties, CP130 provided better protection from ischaemia/reperfusion injury at the histological level. Synthetic iron chelators may therefore be of benefit in clinical organ transplantation by protecting against tissue damage caused by prolonged ischaemia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effect of a synthetic hexadentate iron chelator (CP130) and desferrioxamine on rabbit kidneys exposed to cold and warm ischaemia

et al. 1993

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“…It has been shown that reactive oxygen species (ROS) play an important role in this type of injury and that activated neutrophils, vascular endothelial mitochondria and activated xanthine oxidase are sources of ROS. Especially, the electron transport system of mitochondria is thought to be the main source of intracellular oxygen radicals during reoxygenation [6,8,9]. Thus the vascular endothelial mitochondria play an important role not only in the synthesis of high-energy phosphate compounds but also in the onset of and recovery from ischemia-reperfusion injuries in tissues.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Injuries in Rat Lungs Preserved for 17 h: An Ultrastructural Study

Ueda

Kosaka²,

Hirata³

et al. 1999

Eur Surg Res

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Mitochondria of the small vasculature endothelial cells were examined in preserved rat lungs before and after reperfusion, and the ultrastructural changes were correlated with pulmonary function after reperfusion. Rat lungs were flushed with perfusate and prostaglandin E1 and divided into five groups (n = 5 in each group): group A, normal control group; group B, University of Wisconsin solution; group C, Euro-Collins solution; group D, ET-Kyoto solution, and group E, new ET-Kyoto solution. After preservation at 4°C for 17 h, the left lungs were reperfused at 37°C for 60 min. Tissue was sampled and mitochondria of the small vasculature endothelial cells were ultrastructurally analyzed by transmission electron microscopy before and after reperfusion. The ultrastructure of the mitochondria was well maintained in groups A, B and E before and after reperfusion. In group C, the number of severely degenerated mitochondria in the sectional area of 100 μm² before reperfusion was 18.0 ± 3.9, which was significantly larger than in the other groups (p < 0.01), and the total number of mitochondria significantly decreased with reperfusion (from 24.8 ± 3.5 to 8.2 ± 2.4, p < 0.05). In group C, the shunt fraction, mean pulmonary arterial pressure and the wet-dry ratio of the lung tissue after reperfusion C were significantly higher than in the other groups (p < 0.05; 76.3 ± 1.5%, 54.8 ± 4.2 mm Hg, and 20.6 ± 2.5, respectively). A positive correlation was found between the percentage of the mitochondrial degeneration before reperfusion and the physiological parameters after reperfusion. Mitochondrial damage associated with cold ischemia is probably involved in lung injury caused by cold preservation and reperfusion.

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“…Oxygen free radicals may damage phospholipid membranes. 22,37,38 Once the cellular membranes are ruptured, the cells exhibit necrosis. Furthermore, ischemia causes swelling because the cells cannot maintain an appropriate ion gradient across their membranes.…”

Section: Discussionmentioning

confidence: 99%

Cell proliferation and death of growth plate chondrocyte caused by ischemia and reperfusion

et al. 2001

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Lipid Peroxidation and Ultrastructural Changes in Rat Lung Isografts After Single-Passage Organ Flush and 48-Hour Cold Storage With and Without One-Hour Reperfusion in Vivo

Cited by 26 publications

References 0 publications

The effect of a synthetic hexadentate iron chelator (CP130) and desferrioxamine on rabbit kidneys exposed to cold and warm ischaemia

The effect of a synthetic hexadentate iron chelator (CP130) and desferrioxamine on rabbit kidneys exposed to cold and warm ischaemia

Mitochondrial Injuries in Rat Lungs Preserved for 17 h: An Ultrastructural Study

Cell proliferation and death of growth plate chondrocyte caused by ischemia and reperfusion

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