Effect of Adrenocorticotrophic Hormone and Cortisone on the Uptake of Tritiated Thymidine by Regenerating Liver Tissue in the White Rat

Guzek, Jan W.

doi:10.1038/201930a0

Cited by 26 publications

(9 citation statements)

References 3 publications

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“…The demonstration in the present study, by direct measurement of DNA accretion rate, that, in contrast to normally growing weanling liver, the suppression of DNA synthesis in regenerating liver is at best incomplete is at variance with the conclusions of a number of recent studies in which an effect upon radioactive thymidine incorporation was the sole index of DNA synthesis examined (15)(16)(17). Rizzo et al, for example, showed that the characteristic peak of [ 3 H]thymidine incorporation normally observed in a regenerating remnant 24 h after partial hepatectomy can be abolished if hydrocortisone is given 6 h before the radioactive precursor and concluded that the hormone can induce a virtually complete suppression of regeneration.…”

Section: Discussioncontrasting

confidence: 71%

Suppression of Liver Cell Proliferation by Glucocorticoid Hormone: A Comparison of Normally Growing and Regenerating Tissue in the Immature Rat*

et al. 1978

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The influence of glucocorticoid hormone on the time-course of liver regeneration in the immature rat has been studied by direct measurement of the rate of DNA accretion after the stimulus of partial hepatectomy. In contrast to hepatocyte proliferation associated with normal growth, which almost completely abolished by small doses of glucocorticoid, it is shown that even enormous amounts of hormone produce, at most, about a halving of the intrinsic cell proliferation rate in regenerating liver. Although deceptively magnified by the exponential growth pattern of the hepatic remnant, the inhibition of cell proliferation is thus considerably less complete than that induced in normally growing liver by much lower doses of hormone, a finding at distinct variance with the conclusions of earlier studies based entirely upon observations of radioactive precursor incorporation rather than direct measurement of DNA accretion. The mechanism by which a regenerative stimulus causes hepatocyte proliferation to lose its normal sensitivity to suppression by glucocorticoid, and thereby to exhibit a steroid insensitivity characteristic of other tissues in which cell proliferation reflects cell replenishment rather than normal growth, remains unknown.

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Section: Discussioncontrasting

confidence: 71%

Suppression of Liver Cell Proliferation by Glucocorticoid Hormone: A Comparison of Normally Growing and Regenerating Tissue in the Immature Rat*

et al. 1978

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“…Glucocorticoid action is not so definitely known, except perhaps on lymphatic tissue [12,13,15,16,19,26]; however, it is known that glu cocorticoids have, in general, a catabolic effect, opposite to that of an drogens, and inhibit protein synthesis. Furthermore, it has recently been shown that glucocorticoids inhibit erythropoiesis in normal rats [7,10].…”

Section: Discussionmentioning

confidence: 99%

Aplastic Anemia: Some Clinical and Laboratory Aspects and an Evaluation of the Androgen-Glucocorticoid Treatment

Corneo¹,

Cortellaro²,

Maiolo³

1971

Acta Haematol

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Some clinical aspects in 18 patients affected by aplastic anemia are considered. Liver involvement might be due to serum hepatitis, drug toxicity and possibly to the same etiologic factors causing aplastic anemia. In some patients a decreased glucose tolerance has been found. Serum immunoglobulin levels were normal in the majority of the patients. In one patient there was hypogammaglobulinemia and in a few patients hypergammaglobulinemia in the absence of liver diseases and infections. Concerning therapy, androgens appear to be beneficial, while glucocorticoids were unuseful and in several occasions dangerous.

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“…Additionally, liver regeneration recently has been conceptualized as a phenomenon regulated by T lymphocytes (27,28). In fact, regeneration is inhibited rather than enhanced by nonspecific immunosuppressive agents such as azathioprine (29) and glucocorticoids (30).…”

Section: Discussionmentioning

confidence: 99%

FK 506 ameliorates the hepatic injury associated with ischemia and reperfusion in rats

et al. 1991

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The effect of FK 506 on regeneration of the liver was studied in rats after a two-thirds partial hepatectomy after 60 min of ischemia of the unresected liver. The animals were divided into three distinct groups of 10 rats each. Group 1 (controls) received 0.5 ml saline solution intravenously 30 min after the induction of ischemia. Groups 2 and 3 were injected with FK 506 (0.3 mg/kg) intravenously 30 min after and 24 min before the induction of hepatic ischemia, respectively. The hepatic content of ATP and serum levels of ALT and lactate dehydrogenase were determined on each animal. In addition, the histological appearance and mitotic activity of the remnant liver was determined at regular 24-hr intervals after hepatic ischemia. All 10 control animals died within 72 hr. Treatment with FK 506 resulted in improved survival in groups 2 and 3 (30% and 80%, respectively). The improved survival seen in the FK 506-treated animals was reflected by a restoration of hepatic ATP content, a reduction in the serum levels of ALT and lactate dehydrogenase, an amelioration of hepatic necrosis and neutrophilic infiltration and an increase in the mitotic activity of the liver. These results suggest that FK 506 ameliorates the hepatic injury associated with ischemia/ reperfusion and has a potent stimulatory effect on liver cell regeneration that may make it valuable as a hepatoprotective agent when administered to organ donors before graft harvesting.In recent years, orthotopic liver transplantation (OLT) has been accepted as a reasonable therapy for patients with end-stage liver disease (1). However, the allograft liver is subject to a variety of insults as a result of ischemia experienced during the organ harvest, reperfusion at the time of organ engraftment, and eventually as part of the recipient's immunological response to the allograft after transplantation. The ability of the liver to withstand these injuries and then to regenerate and regulate its ultimate size is crucial after clinical liver transplantation.Recently, it has been reported that FK 506 (FK), in addition to being a powerful immunosuppressive agent, is also hepatotrophic agent (2,3). To further clarify this issue, this study was performed. Specifically the efficacy of FK in protecting the liver against the injury associated with ischemia/reperfusion in rats subjected to a two-thirds hepatectomy after 60-min of ischemia was examined. MATERIALS AND METHODS Surgical ProcedureAdult male Lewis rats weighing between 200 and 300 gm were used in the study. Anesthesia was induced using ether and was maintained with inhalation of metofane. Through a midline abdominal incision a 60-min period of ischemia of the right lateral lobe of the liver was induced by placing noncrushing microvascular clamps around the appropriate branches of the portal vein and hepatic artery using an operative microscope. On releasing the clamps and restoring blood flow to the right lateral lobe, the median and left lateral lobes of the liver were excised according to the method of Higgin...

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Effect of Adrenocorticotrophic Hormone and Cortisone on the Uptake of Tritiated Thymidine by Regenerating Liver Tissue in the White Rat

Cited by 26 publications

References 3 publications

Suppression of Liver Cell Proliferation by Glucocorticoid Hormone: A Comparison of Normally Growing and Regenerating Tissue in the Immature Rat*

Suppression of Liver Cell Proliferation by Glucocorticoid Hormone: A Comparison of Normally Growing and Regenerating Tissue in the Immature Rat*

Aplastic Anemia: Some Clinical and Laboratory Aspects and an Evaluation of the Androgen-Glucocorticoid Treatment

FK 506 ameliorates the hepatic injury associated with ischemia and reperfusion in rats

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