Lipid peroxidation is a nonparenchymal cell event with reperfusion after prolonged liver ischemia

Walsh, Thomas; Rao, Prakash; Makowka, Leonard; Starzl, Thomas E.

doi:10.1016/0022-4804(90)90104-a

Cited by 38 publications

(12 citation statements)

References 30 publications

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“…However, most researchers agree that oxygen-derived free radicals formed during reperfusion are important elements of this injury. These radicals are believed to be involved in lipid peroxidation (3), protein oxidation (4), and cross-linking (5), and as signals for other injurious processes such as neutrophil chemotaxis (6)(7)(8) and concomitant microvascular blockade (9,10).…”

Section: Introductionmentioning

confidence: 99%

Rapid conversion to high xanthine oxidase activity in viable Kupffer cells during hypoxia.

Wiezorek¹,

Brown²,

Kupperman³

et al. 1994

J. Clin. Invest.

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Section: Introductionmentioning

confidence: 99%

Rapid conversion to high xanthine oxidase activity in viable Kupffer cells during hypoxia.

Wiezorek¹,

Brown²,

Kupperman³

et al. 1994

J. Clin. Invest.

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“…[31], a-tocopherol improved the 30 days' survival of rats after 90 min of ischemia from 0 to 45 %; it is possible that the protective effect of a-tocopherol against free radical injury was less obvious in our study, using shorter periods of ischemia (45 min); hepatocytes are well supplied with antioxidants [21,55], thus, the periods of ischemia might need to be longer to demonstrate a free radical injury that could be ameliorated by the protective effect of antioxidants.…”

Section: N-acetylcysteine (Nac)mentioning

confidence: 78%

Free radical scavengers to prevent reperfusion injury following experimental warm liver ischaemia. Is there a real physiological benefit?

et al. 1999

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Free radical scavengers have been utilized to prevent the consequences of ischemia, however, results do not seem conclusive. In our study we analyzed the blood flow, function, and histology of rat liver tissue after warm liver ischemia, in order to assess the effect of free radicals in liver reperfusion injury. N-acetyl cysteine (NAC), tocopherol, allopurinol, and superoxide dismutase (SOD), pharmacological agents expected to protect from injury mediated by free radicals, were investigated. Laser Doppler flowmetry and photometry were utilized to measure post-ischemic microcirculatory changes as an expression of ischemia-reperfusion injury in a model of segmental liver ischemia in the rat, with an ischemic time of 45 min. Galactose elimination capacity, ALT and histology were used to assess the functional and morphological consequences of ischemia after 24 h of reperfusion. The overall mean blood flow over 1 hour after reperfusion was of 33.9% (SD 11.2) of the normal, non-ischemic control. NAC (31.2 Yo SD 10.9) did not show any protective effect and in some cases the effect seemed to be negative. Tocopherol (41.7 % SD 5.1) marginally improved post ischemic liver tissue blood flow. Treatment with allopurinol did not show any beneficial effects (37.5 % SD 14.2). Only animals treated with SOD showed an improvement of the post ischemic liver microcirculation (57.9 Yo SD 14.4)(P < 0.001) and function. Only SOD produced statistically significant differences in galactose elimination capacity, compared with those of the ischemic control group. This moderately protective effect of SOD is encouraging, however, the relevance of all these compounds in a broader pathophysiological setting remains unproven.

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“…However, hepatocytes have been shown to be relatively resistant to injury by oxygen radicals. After reperfusion of a rat liver following more than 60 min of warm ischemia, lipid peroxidation products were detected only in nonparenchymal cells [12]. Isolated hepatocytes were directly injured by stimu-lated neutrophils.…”

Section: Discussionmentioning

confidence: 95%

Activation of Intracellular Neutrophil Elastase in the Transplantation of Ischemic Liver

Otsuka

Takada²,

Fukunaga³

et al. 2001

Eur Surg Res

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Ischemia-reperfusion injury is an important cause of primary nonfunction of transplanted organs, and neutrophil elastase has been implicated in the pathophysiology of ischemia-reperfusion injury. We assessed the kinetics of intracellular neutrophil elastase (INE) activity in canine liver transplantation. Mongrel dogs underwent orthotopic whole-liver transplantation. The animals in group I (n = 6) received fresh liver grafts, and all of the dogs survived longer than 24 h. The animals in group II (n = 5) received liver grafts injured by 30 min of warm ischemia. Only 1 animal survived longer than 24 h after reperfusion. A significant increase in the serum ALT and LDH levels was observed in group II after reperfusion of the graft. Isolated peripheral neutrophils were homogenized, and the neutrophil elastase activity in the supernatant was determined by using a spectrophotometric assay. The INE activity was expressed as the neutrophil elastase value per 1 × 10¹⁰ peripheral neutrophils. In group I, the INE activity 10 min and 2 h after reperfusion was 7.6 ± 2.6 and 6.1 ± 2.4 U, respectively. In group II, this activity was 25.9 ± 7.4 and 44.3 ± 23.7 U, respectively. There was a significant correlation between serum LDH levels and INE activity 10 min after reperfusion (γ = 0.70, p < 0.02). In conclusion, the INE activity increased more sharply after the reperfusion of ischemically injured liver grafts. The INE activity correlates with serum LDH levels immediately after reperfusion, suggesting that the increase in the INE activity depends on the severity of ischemic damage.

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Lipid peroxidation is a nonparenchymal cell event with reperfusion after prolonged liver ischemia

Cited by 38 publications

References 30 publications

Rapid conversion to high xanthine oxidase activity in viable Kupffer cells during hypoxia.

Rapid conversion to high xanthine oxidase activity in viable Kupffer cells during hypoxia.

Free radical scavengers to prevent reperfusion injury following experimental warm liver ischaemia. Is there a real physiological benefit?

Activation of Intracellular Neutrophil Elastase in the Transplantation of Ischemic Liver

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