Adenylate energy charge and cytochrome a (+a3) in the cirrhotic rat liver

Jikko, Akira; Taki, Yoshiro; Nakamura, Noriaki; Tanaka, Junji; Kamiyama, Yasuo; Ozawa, Kazue; Tobe, Takayoshi

doi:10.1016/0022-4804(84)90201-4

Cited by 45 publications

(12 citation statements)

References 15 publications

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“…On the other hand, previous and recent studies from our laboratory have focused on the compensatory responses of liver mito chondria to metabolic derangements such as those occurring after major hepatectomy, jaundice, hemorrhagic shock and liver cir rhosis [9,16,24,26]. These results have shown that KBR is positively correlated with the hepatic energy charge levels.…”

Section: Discussionsupporting

confidence: 62%

Changes in Energy Metabolism of Allografts after Liver Transplantation

Morimoto

Ukikusa²,

Taki³

et al. 1988

Eur Surg Res

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To evaluate the function of energy metabolism in allografts after liver transplantation, changes in hepatic energy charge levels, oxidative and phosphorylative activities of mitochondria and arterial blood ketone body ratio (acetoacetate/3-hydroxybutyrate; KBR) were studied in piglets. Hepatic energy charge levels decreased to 0.831 ± 0.010 at 3 days and 0.836 ± 0.009 at 3 weeks after operation compared to the preoperative value of 0.868 ± 0.006 (p < 0.01), and returned to 0.856 ± 0.007 at 6 weeks. Mitochondrial oxidative and phosphorylative activities were moderately enhanced to 19.14 ± 2.07 (10^–10 mol ATP/mg of mitochondrial protein/s) at 3 days and 20.89 ± 1.72 at 3 weeks compared to the preoperative value of 16.74 ± 2.36, and returned to 16.65 ± 1.54 at 6 weeks. There was no significant difference in the concentrations of mitochondrial respiratory components, except in cytochrome c + c₁. KBR decreased immediately at the beginning of the anhepatic phase and rapidly recovered to the preoperative level within 60 min after revascularization of allografts. There was no change in KBR during the postoperative course except in cases with clinical deterioration. From these results, it is suggested that the mitochondrial capacity for ATP synthesis was enhanced to compensate for the decreased energy charge level and that a decreased KBR is a sign of a critically deranged metabolic function in allografts.

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Section: Discussionsupporting

confidence: 62%

Changes in Energy Metabolism of Allografts after Liver Transplantation

Morimoto

Ukikusa²,

Taki³

et al. 1988

Eur Surg Res

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“…Male albino rats of Wistar strain, weighing 200-220 g, were injected s.c. with 0.4 ml carbon tetrachloride (diluted 1 : 4 with olive oil) per kilogram of body weight twice a week for 3-4 months with free access to phenobarbitone solution (0.5 g/1 water) [8]. Since cirrhotic rats thus obtained grew to about 240-300 g b.wt., normal rats of the same weight were used in the experiments.…”

Section: Animal Modelsmentioning

confidence: 99%

“…), fixed snugly on a surgical board in a supine position and allowed to breathe spontaneously without a respirator. Liver cirrhosis was confirmed by macroscopic appearance, ascites, and elevated concentration of cytochrome a (+ as) [8]. A 24-gauge plastic catheter was inserted into the right common iliac artery and 50 U heparin sodium were injected into the artery immediately after cannulation.…”

Section: Animal Modelsmentioning

confidence: 99%

Influence of hypoxia on mitochondrial function and energy status in CCl4-induced cirrhotic rat liver

Sugiyama

Ikai

et al. 1989

Res. Exp. Med.

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The influence of hypoxia on hepatic mitochondrial function and energy status was studied in normal and carbon tetrachloride (CCl4)-induced cirrhotic rats. Under hypoxemia of 50 mm Hg-PaO2, hepatic energy status was suppressed both in normal and cirrhotic rats. After the reversal of hypoxia, it was completely restored in normal rats concomitant with a rapid elevation of hepatic mitochondrial redox state (overshoot phenomenon) and increase in the mitochondrial oxidative phosphorylative activity. By contrast, in cirrhotic rats, such an enhancement of mitochondrial function was not observed. It was clarified that cirrhotic liver mitochondrial function was not observed. It was clarified that cirrhotic liver mitochondria have little capacity to respond to the hypoxic stress. A lower resistance to hypoxic episode in cirrhotics might be attributable to the absence of mitochondrial enhancement which is a compensatory mechanism for the deranged energy metabolism of the liver.

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“…Darüberhinaus sind die cirrhotischen Lebern sehr anfällig für Ischämie-Reperfusionsschädigung. Studien haben gezeigt, dass die mitochondrialen Systeme in cirrhotischen Lebern beeinträchtigt sind, was zu cellulären Energiekrisen unter Ischämie führt [7]. Durch irreguläre sinusoidale Verhältnisse kann die Mikrozirkulation, sogar nach kurzzeitiger Ischämie, während der Reperfusion besonders leicht beeinträchtigt werden.…”

Section: Allgemeine Problemeunclassified

Leberresektion bei Lebercirrhose

Yamamoto

2001

Chirurg

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The benefits of liver resection for patients with hepatocellular carcinoma (HCC) and concomitant liver cirrhosis have been questionable due to high rates of postoperative complications. As a result of advance in surgical techniques, along with improved perioperative management and increased knowledge of the pathophysiology of liver cirrhosis, liver resection in cirrhotic patients has become a safer surgical procedure during the 1990s. This article introduces our techniques of parenchymal resection in patients with liver cirrhosis, avoiding inflow occlusion of the hepatic circulation by using a Cavitron Ultrasonic Surgical Aspirator (CUSA) and bipolar cautery that is equipped with a mechanism for channeling water at the point of cauterization. Analysis of survival rates showed that surgical resection was more advantageous than treatment such as percutaneous ethanol injection, although the discovery of multicentric carcinogenesis in livers with hepatitis C viral infection required us to reconsider surgical indications for HCC and concomitant liver cirrhosis.

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Adenylate energy charge and cytochrome a (+a3) in the cirrhotic rat liver

Cited by 45 publications

References 15 publications

Changes in Energy Metabolism of Allografts after Liver Transplantation

Changes in Energy Metabolism of Allografts after Liver Transplantation

Influence of hypoxia on mitochondrial function and energy status in CCl4-induced cirrhotic rat liver

Leberresektion bei Lebercirrhose

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