The Effects of Adrenalectomy and Hypophysectomy on Bile Flow in the Rat

Bauman, J.D.; Chang, Beom Seok; Hall, FS

doi:10.1530/acta.0.0520404

Cited by 27 publications

(21 citation statements)

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“…Systematic evaluation of the influence of adrenocortical steroids on biliary composition and flow in normal experimental animals appears to be lacking (10)(11)(12). In the studies presented herewith, the effects of intravenous hydrocortisone on bile formation during constant taurocholate infusion have been explored in unanesthetized dogs equipped with duodenal cannulae.…”

Section: Introductionmentioning

confidence: 99%

Hydrocortisone choleresis in the dog

Macarol¹,

Morris²,

Baker³

et al. 1970

J. Clin. Invest.

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A B S T R A C T Hydrocortisone sodium succinate (SoluCortef; Upjohn Co., Kalamazoo, Mich.) has been found to induce choleresis in unanesthetized fasting dogs fitted with Thomas duodenal cannulae for direct quantitative collection of bile. In all experiments, bile flow increased (average, 68%) 15-20 min after beginning hydrocortisone by infusion in association with an equivalent increment in the output of sodium, potassium, chloride, and bicarbonate. In five animals, the choleretic response occurred independently of, and apparently additive to, the effect of simultaneously administered sodium taurocholate. The fluid added to the bile resembled an ultrafiltrate of plasma. Erythritol clearance increased in proportion to flow, suggesting an effect at the hepatocellular rather than ductal level and probably independent, therefore, of endogenous secretin release. Hydrocortisone and its metabolites were excreted in amounts too small to induce choleresis osmotically. Simultaneous administration of sulfobromophthalein sodium blocked the choleretic response without preventing hydrocortisone excretion. The data suggest that a previously ill-defined mechanism of canalicular bile formation, not mediated by bile salt excretion, may be operative in choleretic response to a variety of agents.

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Section: Introductionmentioning

confidence: 99%

Hydrocortisone choleresis in the dog

Macarol¹,

Morris²,

Baker³

et al. 1970

J. Clin. Invest.

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“…The usual pattern described in CPHD is "giant cell hepatitis" (5,8,13,21). In our patients who showed physical findings consistent with hypopituitarism, liver biopsies were not carried out, assuming that the cholestasis was potentially a manifestation of hormone deficiencies (4,14,19).…”

Section: Discussionmentioning

confidence: 90%

“…Since the initial report of CPHD in an infant with cholestasis and hypoglycemia by Blizzard and Alberts (7), several descriptions of case reports and few case series have been described. Although it is not exactly known how hormone deficiencies cause cholestasis, the evidence of clinical and some experimental data supports the role of pituitary trophic hormones (cortisol, GH and thyroid hormones) in the pathogenesis of this disorder (8)(9)(10)(11)(12)(13). Cortisol deficiency in adrenalectomized animals reduces biliary flow, which is reverted after treatment with hydrocortisone.…”

Section: Discussionmentioning

confidence: 99%

Neonatal cholestasis in congenital pituitary hormone deficiency and isolated hypocortisolism: characterization of liver dysfunction and follow-up

Braslavsky

Keselman

Galoppo

et al. 2011

Arq Bras Endocrinol Metab

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INTRODUCTION: Neonatal cholestasis due to endocrine diseases is infrequent and poorly reco-gnized. Referral to the pediatric endocrinologist is delayed. OBJECTIVE: We characterized cholestasis in infants with congenital pituitary hormone deficiencies (CPHD), and its resolution after hormone replacement therapy (HRT). SUBJECTS AND METHODS: Sixteen patients (12 males) were included; eleven with CPHD, and five with isolated central hypocortisolism. RESULTS: Onset of cholestasis occurred at a median age of 18 days of life (range 2-120). Ten and nine patients had elevated transaminases and γGT, respectively. Referral to the endocrinologist occurred at 32 days (range 1 - 72). Remission of cholestasis occurred at a median age of 65 days, whereas liver enzymes occurred at 90 days. In our cohort isolated, hypocortisolism was a transient disorder. CONCLUSION: Cholestasis due to hormonal deficiencies completely resolved upon introduction of HRT. Isolated hypocortisolism may be a transient cause of cholestasis that needs to be re-evaluated after remission of cholestasis.

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“…Braslavsky'dan farklı olarak GH başlandıktan 70 gün, postnatal 120. gününde kolestazı düzel-miştir. Konjenital hipofiz hormon eksikliğinde hangi hormon eksikliğinin kolestaza neden olduğu bilinmemektedir (5). Adrenalleri alınan hayvanlarda kortizol eksikliği ile safra akımı-nın azaldığı gösterilmiştir.…”

Section: Discussionunclassified