Some aspects of glycogen metabolism following reversible or irreversible liver ischemia

Bernelli‐Zazzera, Aldo; Gaja, G.

doi:10.1016/0014-4800(64)90007-3

Cited by 66 publications

(15 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For the in vivo warm ischemia, inflow to the median and left lateral lobes were occluded with a microvascular clip for 90 minutes. 13 The abdominal skin was closed during the period of ischemia. At the end of 90 minutes, the vascular clip was removed, and the abdomen was closed in layers.…”

Section: Methodsmentioning

confidence: 99%

Oxidative Stress in Fatty Livers of Obese Zucker Rats: Rapid Amelioration and Improved Tolerance to Warm Ischemia With Tocopherol

2001

View full text Add to dashboard Cite

Fatty livers in humans and rats are less tolerant of ischemia, endotoxin, and alcohol. We hypothesized that fatty livers of obese (Ob) Zucker rats are oxidatively stressed and oxidative stress could be relieved by antioxidant treatment, leading to improved tolerance to ischemia. Total glutathione (GSH), tocopherol (TOC), ascorbic acid (AA), catalase (CAT), superoxide dismutase (SOD), and selenium-glutathione peroxidase (Se-GPx) were measured in the livers of Ob and lean (Ln) Zucker rats before and after treatment with high-dose TOC and ascorbate. Also, survival in treated Ob rats following a lethal 90 minutes of partial in vivo warm ischemia was examined. Fatty livers of Ob rats contained significantly less GSH, TOC, and CAT, in comparison with livers of Ln rats. Immunoblotting showed significantly decreased CAT protein without changes in mRNA in fatty livers. There were no significant differences in AA, SOD, and Se-GPx between the 2 groups. Pretreatment with TOC and ascorbate over 48 hours completely corrected the decreases in GSH, TOC, and CAT. Most importantly, TOC with or without ascorbate pretreatment significantly improved survival in Ob rats following ischemia in a dosedependent manner. Fatty livers in humans and experimental animals are more prone to a variety of insults such as ischemia/reperfusion (I/ RP), endotoxin, and alcohol. Nonalcoholic steatohepatitis and its progression to cirrhosis are well-defined clinical entities. 1 Recipients of human donor livers with moderate or severe steatosis have decreased graft and patient survival. 2 Although exact figures are not available, it is believed that as many as 30% of donor livers have varying degrees of steatosis on routine microscopic examination. About 10% of donor livers are not used for transplantation because of moderate to severe steatosis, and this worsens the current shortage of livers. 2 Treatment regimens that will improve tolerance of fatty livers to the aforementioned insults are needed, and would benefit a diverse group of patients.Two rodent models of fatty liver, the genetically obese (Ob) and lipotrope-deficient diet models, are used in the laboratory to further investigate the problems associated with fatty livers. Abnormalities in sinusoidal microcirculation, 3,4 mitochondrial oxidative phosphorylation including a decrease in adenosine triphosphate production, 5,6 and dysregulation of cytokine production 7 are some of the mechanisms that have been associated with the increased injury to fatty livers in both rodents and humans. Oxidative stress has recently been postulated to be a common feature in fatty livers of diverse etiologies. 1 Lipid peroxidation products in the liver are increased in both models of rat fatty liver. 8,9 Reactive oxygen intermediates are key mediators of I/RP injury in solid organs. Thus, a 2-step oxidative injury comprised of a chronic oxidative stress before and an additional acute oxidative stress following I/RP may explain the increased injury sustained by fatty livers following both cold and warm ischemia.To...

show abstract

Section: Methodsmentioning

confidence: 99%

Oxidative Stress in Fatty Livers of Obese Zucker Rats: Rapid Amelioration and Improved Tolerance to Warm Ischemia With Tocopherol

2001

View full text Add to dashboard Cite

show abstract

“…that hyperglycemia takes place after reflow of ischemic liver [4,8,28] which may induce a release of insulin. Another possibility is a release of unknown factor(s) from the isch emic lobe upon reflow, leading to mitochon drial enhancement.…”

Section: Discussionmentioning

confidence: 99%

“…The liver of mam mals can tolerate up to 30-60 min of isch emia and still resume normal functioning after recirculation of oxygenated blood [3,4,6,9]. Different species have different time limits for the reversibility of impaired he patic function due to their dissimilar vascu lar anatomy of the liver [7], Moreover, even within the same species, there is no absolute point beyond which cellular changes become irreversible because of differences in strain, diet and biological factors [4,21,32].…”

Section: Introductionmentioning

confidence: 99%

Effects of Partial Ischemia and Reflow on Mitochondrial Metabolism in Rat Liver

et al. 1988

View full text Add to dashboard Cite

To clarify the effects of partial ischemia and reflow on the mitochondrial metabolism of the rat liver, the afferent vessels supplying the left lateral and left half of medial lobes were occluded and then reperfused after given time periods of ischemia (30, 60, 90 and 120 min, groups A, B, C and D, respectively). Samplings were taken at 0, 10 and 60 min after reperfusion. The energy charge levels of ischemic lobes decreased rapidly from 0.85 ± 0.01 in the sham group to 0.38 ± 0.11, 0.35 ± 0.07 and 0.34 ± 0.06 in groups B, C and D, respectively. The phosphorylative activities of mitochondria isolated from ischemic lobes decreased gradually along with the time of ischemia. The reversal of mitochondrial function and energy charge levels following reperfusion was noted in groups A and B. In nonischemic lobes, the phosphorylation rate (nmol ATP/mg/min) increased from 90 ± 6 in sham group to 125 ± 12 and 130 ± 9; 131 ± 5 and 130 ± 6; 123 ± 6 and 122 ± 17, and 138 ± 6 and 138 ± 13 at 10 and 60 min after reflow in groups A, B, C and D, respectively (p < 0.05). The energy charge level of nonischemic lobes decreased from 0.85 ± 0.01 of sham group to 0.80 ± 0.03 in group D (p < 0.05). From these results, it is concluded that the transitional zone for the reversal of mitochondrial function and energy metabolism following prolonged liver ischemia appears at around 60 min. It is suggested that there exist some mechanism(s) which lead to an enhancement of mitochondrial function in nonischemic lobe after reflow.

show abstract

“…Male Wistar rats of 250 g, housed and handled as prescribed by EC regulations, were used throughout and were subjected to partial liver ischemia of 1 h duration as described [10]. After different times of reperfusion the rats were killed, the livers were rapidly excised and deep frozen.…”

Section: Animals and Treatmentmentioning

confidence: 99%

“…Liver ischemia can cause severe cell damage without leading to cell death if not too prolonged [10]. On the other hand, reperfusion can induce oxidative stress [11], the release of proinflammatory cytokines by Kupffer cells [12,13] and various biochemical processes [14] including the reprogramming of gene expression with a rapid induction of c-fos, c-jun and stress genes [15].…”

Section: Introductionmentioning

confidence: 99%

The MAP kinase cascades are activated during post‐ischemic liver reperfusion

et al. 1996

View full text Add to dashboard Cite

We have investigated the involvement of MAP kinase cascades in the response of the liver to post-ischemic reperfusion. Both JNKs and ERKs are activated but the duration and magnitude of the increase in their activities appear to be different. JNK activation is more marked but shorter than that of ERKs. The increase observed in the phosphotyrosine content of the 52 kDa Shc protein, accompanied by an increased amount of co-immunoprecipitated Grb2, and the activation of Raf-1 kinase provide evidence of the involvement of a Ras-Rafdependent pathway, with a time course that is similar to that of ERK activation. The treatment of rats with IL-1 receptor antagonist modified all of the described effects, suggesting that IL-1 plays a role in the response of the liver to reperfusion.

show abstract

Some aspects of glycogen metabolism following reversible or irreversible liver ischemia

Cited by 66 publications

References 20 publications

Oxidative Stress in Fatty Livers of Obese Zucker Rats: Rapid Amelioration and Improved Tolerance to Warm Ischemia With Tocopherol

Oxidative Stress in Fatty Livers of Obese Zucker Rats: Rapid Amelioration and Improved Tolerance to Warm Ischemia With Tocopherol

Effects of Partial Ischemia and Reflow on Mitochondrial Metabolism in Rat Liver

The MAP kinase cascades are activated during post‐ischemic liver reperfusion

Contact Info

Product

Resources

About