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Low-dose ethanol attenuates gut ischemia/reperfusion-induced liver injury in rats via nitric oxide production.
J Gastroenterol Hepatol. 2003 Feb; 18(2):211-7.JG

Abstract

BACKGROUND AND AIMS

The acute administration of low-dose ethanol was demonstrated to attenuate liver injury elicited by gut ischemia/reperfusion (I/R). Nitric oxide (NO) has been found to be a modulator of adhesive interactions between leukocytes, platelets, and endothelial cells, but there has been much controversy about the effects of ethanol on NO regulation. The objective of this study was to investigate the role of NO in ethanol-reduced hepatic microvascular dysfunction elicited by gut I/R.

METHODS

Male Wistar rats were exposed to 30 min of gut ischemia followed by 60 min of reperfusion. Intravital microscopy was used to monitor leukocyte recruitment and non-perfused sinusoids (NPS). Plasma alanine aminotransferase (ALT) activities were measured 6 h after the onset of reperfusion. In another set of experiments, ethanol (10%, 1 g/kg) was administered before ischemia.

RESULTS

Gut I/R elicited increases in the number of stationary leukocytes, NPS, and plasma ALT activities; all of which were attenuated by pretreatment with ethanol or an NO donor. Gut I/R caused the apoptosis of hepatocytes, which was prevented by pretreatment with ethanol. Pretreatment with an NO synthase inhibitor diminished the protective effects of ethanol. The administration of ethanol increased plasma nitrite/nitrate levels.

CONCLUSION

These results suggest that low-dose ethanol attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential liver injury by increasing sinusoidal NO levels.

Authors+Show Affiliations

Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

12542608

Citation

Horie, Yoshinori, et al. "Low-dose Ethanol Attenuates Gut Ischemia/reperfusion-induced Liver Injury in Rats Via Nitric Oxide Production." Journal of Gastroenterology and Hepatology, vol. 18, no. 2, 2003, pp. 211-7.
Horie Y, Yamagishi Y, Kato S, et al. Low-dose ethanol attenuates gut ischemia/reperfusion-induced liver injury in rats via nitric oxide production. J Gastroenterol Hepatol. 2003;18(2):211-7.
Horie, Y., Yamagishi, Y., Kato, S., Kajihara, M., Kimura, H., & Ishii, H. (2003). Low-dose ethanol attenuates gut ischemia/reperfusion-induced liver injury in rats via nitric oxide production. Journal of Gastroenterology and Hepatology, 18(2), 211-7.
Horie Y, et al. Low-dose Ethanol Attenuates Gut Ischemia/reperfusion-induced Liver Injury in Rats Via Nitric Oxide Production. J Gastroenterol Hepatol. 2003;18(2):211-7. PubMed PMID: 12542608.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Low-dose ethanol attenuates gut ischemia/reperfusion-induced liver injury in rats via nitric oxide production. AU - Horie,Yoshinori, AU - Yamagishi,Yoshiyuki, AU - Kato,Shinzo, AU - Kajihara,Mikio, AU - Kimura,Hiroyuki, AU - Ishii,Hiromasa, PY - 2003/1/25/pubmed PY - 2003/6/25/medline PY - 2003/1/25/entrez SP - 211 EP - 7 JF - Journal of gastroenterology and hepatology JO - J Gastroenterol Hepatol VL - 18 IS - 2 N2 - BACKGROUND AND AIMS: The acute administration of low-dose ethanol was demonstrated to attenuate liver injury elicited by gut ischemia/reperfusion (I/R). Nitric oxide (NO) has been found to be a modulator of adhesive interactions between leukocytes, platelets, and endothelial cells, but there has been much controversy about the effects of ethanol on NO regulation. The objective of this study was to investigate the role of NO in ethanol-reduced hepatic microvascular dysfunction elicited by gut I/R. METHODS: Male Wistar rats were exposed to 30 min of gut ischemia followed by 60 min of reperfusion. Intravital microscopy was used to monitor leukocyte recruitment and non-perfused sinusoids (NPS). Plasma alanine aminotransferase (ALT) activities were measured 6 h after the onset of reperfusion. In another set of experiments, ethanol (10%, 1 g/kg) was administered before ischemia. RESULTS: Gut I/R elicited increases in the number of stationary leukocytes, NPS, and plasma ALT activities; all of which were attenuated by pretreatment with ethanol or an NO donor. Gut I/R caused the apoptosis of hepatocytes, which was prevented by pretreatment with ethanol. Pretreatment with an NO synthase inhibitor diminished the protective effects of ethanol. The administration of ethanol increased plasma nitrite/nitrate levels. CONCLUSION: These results suggest that low-dose ethanol attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential liver injury by increasing sinusoidal NO levels. SN - 0815-9319 UR - https://www.unboundmedicine.com/medline/citation/12542608/Low_dose_ethanol_attenuates_gut_ischemia/reperfusion_induced_liver_injury_in_rats_via_nitric_oxide_production_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0815-9319&date=2003&volume=18&issue=2&spage=211 DB - PRIME DP - Unbound Medicine ER -