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Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: role of nitric oxide synthase isoforms.
J Gastroenterol Hepatol. 2006 Jul; 21(7):1194-9.JG

Abstract

BACKGROUND

Hepatic encephalopathy is a complex neuropsychiatric syndrome. A previous study showed that chronic nitric oxide (NO) inhibition aggravated the severity of encephalopathy in thioacetamide (TAA)-treated rats. The present study investigated the relative contribution of NO synthase (NOS) isoforms on the severity of hepatic encephalopathy in TAA-treated rats.

METHOD

Fulminant hepatic failure was induced in male Sprague-Dawley rats by intraperitoneal injection of TAA (350 mg/kg/day) for 3 days. Rats were divided into three groups to receive N(omega)-nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 25 mg/kg/day in tap water), L-canavanine (an inducible NOS inhibitor, 100 mg/kg/day via intraperitoneal injection) or normal saline (N/S) from 2 days prior to TAA administration and lasting for 5 days. Severity of encephalopathy was assessed by the counts of motor activity. Plasma levels of tumor necrosis factor-alpha (TNF- alpha) were determined by enzyme-linked immunosorbent assay (ELISA), and total bilirubin, alanine aminotransferase (ALT) and creatinine were determined by colorimetric assay.

RESULTS

Compared with L-canavanine or N/S-treated rats (0% and 4%, respectively), the mortality rate was significantly higher in rats receiving L-NAME administration (29%, P < 0.005). Inhibition of NO created detrimental effects on the counts of motor activities (P < 0.05). Rats treated with L-NAME had significantly higher plasma levels of total bilirubin, ALT, creatinine and TNF- alpha as compared with rats treated with L-canavanine or N/S (P < 0.01).

CONCLUSION

Chronic L-NAME administration, but not L-canavanine, had detrimental effects on the severity of hepatic damage and motor activities in TAA-treated rats. These results suggest that constitutive NOS activities play a major protective role in rats with fulminant hepatic failure.

Authors+Show Affiliations

Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16824075

Citation

Chu, Chi-Jen, et al. "Detrimental Effects of Nitric Oxide Inhibition On Hepatic Encephalopathy in Rats With Thioacetamide-induced Fulminant Hepatic Failure: Role of Nitric Oxide Synthase Isoforms." Journal of Gastroenterology and Hepatology, vol. 21, no. 7, 2006, pp. 1194-9.
Chu CJ, Chang CC, Wang TF, et al. Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: role of nitric oxide synthase isoforms. J Gastroenterol Hepatol. 2006;21(7):1194-9.
Chu, C. J., Chang, C. C., Wang, T. F., Lee, F. Y., Chang, F. Y., Chen, Y. C., Chan, C. C., Huang, H. C., Wang, S. S., & Lee, S. D. (2006). Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: role of nitric oxide synthase isoforms. Journal of Gastroenterology and Hepatology, 21(7), 1194-9.
Chu CJ, et al. Detrimental Effects of Nitric Oxide Inhibition On Hepatic Encephalopathy in Rats With Thioacetamide-induced Fulminant Hepatic Failure: Role of Nitric Oxide Synthase Isoforms. J Gastroenterol Hepatol. 2006;21(7):1194-9. PubMed PMID: 16824075.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Detrimental effects of nitric oxide inhibition on hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: role of nitric oxide synthase isoforms. AU - Chu,Chi-Jen, AU - Chang,Ching-Chih, AU - Wang,Teh-Fang, AU - Lee,Fa-Yauh, AU - Chang,Full-Young, AU - Chen,Yi-Chou, AU - Chan,Che-Chang, AU - Huang,Hui-Chun, AU - Wang,Sun-Sang, AU - Lee,Shou-Dong, PY - 2006/7/11/pubmed PY - 2006/11/15/medline PY - 2006/7/11/entrez SP - 1194 EP - 9 JF - Journal of gastroenterology and hepatology JO - J Gastroenterol Hepatol VL - 21 IS - 7 N2 - BACKGROUND: Hepatic encephalopathy is a complex neuropsychiatric syndrome. A previous study showed that chronic nitric oxide (NO) inhibition aggravated the severity of encephalopathy in thioacetamide (TAA)-treated rats. The present study investigated the relative contribution of NO synthase (NOS) isoforms on the severity of hepatic encephalopathy in TAA-treated rats. METHOD: Fulminant hepatic failure was induced in male Sprague-Dawley rats by intraperitoneal injection of TAA (350 mg/kg/day) for 3 days. Rats were divided into three groups to receive N(omega)-nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 25 mg/kg/day in tap water), L-canavanine (an inducible NOS inhibitor, 100 mg/kg/day via intraperitoneal injection) or normal saline (N/S) from 2 days prior to TAA administration and lasting for 5 days. Severity of encephalopathy was assessed by the counts of motor activity. Plasma levels of tumor necrosis factor-alpha (TNF- alpha) were determined by enzyme-linked immunosorbent assay (ELISA), and total bilirubin, alanine aminotransferase (ALT) and creatinine were determined by colorimetric assay. RESULTS: Compared with L-canavanine or N/S-treated rats (0% and 4%, respectively), the mortality rate was significantly higher in rats receiving L-NAME administration (29%, P < 0.005). Inhibition of NO created detrimental effects on the counts of motor activities (P < 0.05). Rats treated with L-NAME had significantly higher plasma levels of total bilirubin, ALT, creatinine and TNF- alpha as compared with rats treated with L-canavanine or N/S (P < 0.01). CONCLUSION: Chronic L-NAME administration, but not L-canavanine, had detrimental effects on the severity of hepatic damage and motor activities in TAA-treated rats. These results suggest that constitutive NOS activities play a major protective role in rats with fulminant hepatic failure. SN - 0815-9319 UR - https://www.unboundmedicine.com/medline/citation/16824075/Detrimental_effects_of_nitric_oxide_inhibition_on_hepatic_encephalopathy_in_rats_with_thioacetamide_induced_fulminant_hepatic_failure:_role_of_nitric_oxide_synthase_isoforms_ L2 - https://doi.org/10.1111/j.1440-1746.2006.04310.x DB - PRIME DP - Unbound Medicine ER -