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PubMed1996

Effect of selective blockade of endothelin ETB receptors on the liver dysfunction and injury caused by endotoxaemia in the rat.

1. We investigated the effects of the selective endothelin (ET)A receptor antagonist BQ-485 and the selective ETB receptor antagonist BQ-788 on circulatory failure, multiple organ dysfunction syndrome (MODS) and the alterations in acid base balance caused by endotoxaemia in the anaesthetized rat. 2. Male Wistar rats were anaesthetized (thiopentone sodium; 120 mg kg-1, i.p.) and received a continuous infusion of vehicle (saline, 0.6 ml kg-1h-1, i.v.), BQ-485 (10 nmol kg-1 min-1, i.v.) or BQ-788 (10 nmol kg-1 min-1, i.v.). Fifteen min later, animals received a bolus injection of either saline (0.9% NaCl, 1 ml kg-1, i.v.) or E. coli lipopolysaccharide (LPS, 10 mg kg-1, i.v.). 3. Injection of LPS resulted in a fall in blood pressure from 115 +/- 4 mmHg (time 0) to 82 +/- 4 mmHg at 360 min (n = 15) as well as a hyporeactivity to the pressor responses to noradrenaline (NA, 1 microgram kg-1, i.v.). Infusion of BQ-788 attenuated the delayed hypotension (at 360 min: 100 +/- 4 mmHg, n = 7; P < 0.05) and significantly enhanced the pressor responses elicited by NA (at 60 to 240 min). In contrast, treatment of LPS-rats with BQ-485 augmented the hypotension (at 360 min), but did not affect the vascular hyporeactivity elicited by endotoxaemia. 4. Endotoxaemia for 360 min resulted in rises in the serum levels of urea and creatinine (indicators of renal failure), glutamate-oxalate-transferase (GOT) and glutamate-pyruvate-transferase (GPT) (indicators of hepatocellular injury), and bilirubin and gamma-glutamyl transferase (gamma GT) (indicators of liver failure) as well as nitrite (indicator of the induction of nitric oxide synthase; iNOS). Treatment of LPS-rats with BQ-788, but not with BQ-485, attenuated the degree of liver injury and failure, while neither BQ-788 nor BQ-485 affected the acute renal failure or the induction of iNOS caused by endotoxin. 5. Endotoxaemia also caused (within 15 min) an acute metabolic acidosis (falls in pH, HCO3-and base excess) which was compensated by hyperventilation (fall in PaCO2). Treatment of LPS-rats with BQ-788 or BQ-485 did not affect the metabolic acidosis caused by LPS. 6. Thus, the selective ETB receptor antagonist BQ-788 attenuated (i) the delayed hypotension, (ii) the vascular hyporeactivity to NA as well as (iii) the degree of hepatocellular injury and dysfunction caused by endotoxin in the anaesthetized rat. In contrast, the selective ETA receptor antagonist did neither attenuate the circulatory failure nor the liver or renal dysfunction associated with endotoxaemia. We propose that the prevention of the hepatocellular dysfunction and injury caused BQ-788 in endotoxaemia is due to an improvement in oxygen delivery to the liver secondary to (i) inhibition of pre-sinusoidal constriction, (ii) inhibition of sinusoidal constriction, and (iii) improvement in perfusion pressure.

Alanine Transaminase↗
PubMed2001

Correction of liver dysfunction in DNA repair-deficient mice with an ERCC1 transgene.

The ERCC1 gene is essential for the repair of UV-induced DNA damage. Unlike most genes in the nucleotide excision repair (NER) pathway, ERCC1 is also involved in recombinational repair. Perhaps for this reason, ERCC1 knockout mice are not a model for the human NER deficiency disorder, xeroderma pigmentosum. Instead, ERCC1 null mice are severely runted and die before weaning from liver failure with accelerated hepatocyte polyploidy that is more reminiscent of a premature ageing disorder. To permit study of the role of ERCC1 in other tissues we have corrected the liver ERCC1 deficiency with a transgene under the control of a liver-specific promoter. The transgene alleviated runting and extended the lifespan. The elevated level of oxidative DNA damage and premature liver polyploidy were reversed and liver function was corrected. A widespread mitochondrial dysfunction was identified and an essential role for ERCC1 in the kidney was also revealed with transgene-containing ERCC1-deficient animals going on to die of renal failure. The nuclei of kidney proximal tubule cells became polyploid in a similar way to the premature liver polyploidy observed in younger ERCC1-deficient animals. We believe that this is a response to the accumulation of endogenous DNA damage in these particularly susceptible tissues which cannot be repaired in ERCC1-deficient animals.

Animals↗
PubMed2005

Herpes simplex virus hepatitis causing acute liver dysfunction and thrombocytopenia in pregnancy.

BACKGROUND: Herpes simplex virus (HSV) hepatitis in pregnant women is a rare condition. We report a case confirmed by liver biopsy and successfully treated with empiric intravenous acyclovir. CASE: A 25-year-old primigravida at 34 weeks of gestation presented with fever, thrombocytopenia, and markedly elevated liver enzymes. The patient was treated empirically and was delivered by cesarean. After delivery failed to correct her condition, a liver biopsy revealed HSV hepatitis. The fetus was unaffected and the patient recovered with an extended course of acyclovir. CONCLUSION: Pregnant women are susceptible to disseminated HSV causing hepatitis. A high index of suspicion is necessary to diagnose HSV hepatitis and begin appropriate treatment with acyclovir. Herpes simplex virus hepatitis should be included in the differential diagnosis for liver failure during pregnancy.

Acyclovir↗
PubMed1990

[Pulmonary tuberculosis with chemotherapy related liver dysfunction].

A retrospective study of the hepatotoxicity of antituberculous drugs was undertaken to establish preventive measures for elevated transaminases by analyzing its clinical courses. Four hundred and forty six patients with normal liver function on admission were enrolled in this study. More than 50% of total 113 cases who showed abnormalities of transaminases were aggravated up to 4th week after administration of drugs, and 80% up to 8th week. The initial values of elevated transaminases did not relate to recovery rate, and could tolerate the additional administration of drugs. However, cases with higher peak values and exacerbation in transaminases showed a tendency of delayed normalization. These results indicate that the chronological observation of transaminases is useful to determine whether or not the antituberculous drugs should be discontinued when hepatic dysfunction occurs. Moreover, they suggest that patients with severe pulmonary tuberculosis may continue chemotherapy with the same regimen under careful observation of liver function even when their transaminase values exceed 100.

Adolescent↗