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The sinusoidal pressure during ischemia-reperfusion injury in perfused mouse liver pretreated with or without L-NAME.
J Surg Res. 2007 May 01; 139(1):30-5.JS

Abstract

BACKGROUND

Hepatic ischemia-reperfusion (I/R) is accompanied by liver weight gain and ascites formation possibly caused by an increase in the sinusoidal pressure, a determinant of hepatic transvascular fluid movement. However, changes in the sinusoidal pressure during hepatic I/R in mice are not known. It is also controversial whether nitric oxide (NO) exerts a beneficial or detrimental effect on hepatic I/R injury. We determined the changes in hepatic sinusoidal pressure and liver weight, and the effect of a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) on I/R injury of isolated mouse liver.

MATERIALS AND METHODS

Isolated liver from 20 male outbred ddY mice was perfused portally with diluted blood (Hct 3%). After pretreatment with L-NAME (100 microm) or D-NAME (100 microm), ischemia was induced at room temperature by occlusion of the inflow line of the portal vein for 1 h followed by 1-h reperfusion in a recirculating manner. The sinusoidal pressure was assessed by the double vascular occlusion pressure (Pdo), and pre- and postsinusoidal resistance was determined. Liver injury was assessed by blood levels of alanine aminotransferase (ALT).

RESULTS

In the d-NAME group (n=7), immediately after reperfusion, the portal pressure increased by 2.8 +/- 0.1 (SE) mmHg, which was accompanied by an increase in Pdo of 1.5 +/- 0.1 mmHg, indicating increases in pre- and postsinusoidal resistance to a similar degree. Then, presinusoidal, but not postsinusoidal, resistance sustained increased until 60 min after reperfusion. Liver weight increased to 0.14 +/- 0.04 g/g liver after reperfusion, followed by a gradual return to baseline. Blood ALT levels increased at 60 min after reperfusion. There were no significant differences in changes in the variables between the D- and L-NAME (n=7) groups. In the time-matched non- I/R control group (n=6), no changes in variables were observed for 2 h.

CONCLUSIONS

Mouse hepatic I/R causes marginal liver weight gain associated with a small and transient increase in the sinusoidal pressure, and nitric oxide does not play any significant roles in this injury.

Authors+Show Affiliations

Department of Physiology, Kanazawa Medical University, Uchinada Ishikawa, Japan. shibamo@kanazawa-med.ac.jpNo 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

17292416

Citation

Shibamoto, Toshishige, et al. "The Sinusoidal Pressure During Ischemia-reperfusion Injury in Perfused Mouse Liver Pretreated With or Without L-NAME." The Journal of Surgical Research, vol. 139, no. 1, 2007, pp. 30-5.
Shibamoto T, Ruan Z, Cui S, et al. The sinusoidal pressure during ischemia-reperfusion injury in perfused mouse liver pretreated with or without L-NAME. J Surg Res. 2007;139(1):30-5.
Shibamoto, T., Ruan, Z., Cui, S., Liu, W., Zhao, Z. S., Takano, H., Kurata, Y., Koizumi, T., & Kubo, K. (2007). The sinusoidal pressure during ischemia-reperfusion injury in perfused mouse liver pretreated with or without L-NAME. The Journal of Surgical Research, 139(1), 30-5.
Shibamoto T, et al. The Sinusoidal Pressure During Ischemia-reperfusion Injury in Perfused Mouse Liver Pretreated With or Without L-NAME. J Surg Res. 2007 May 1;139(1):30-5. PubMed PMID: 17292416.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The sinusoidal pressure during ischemia-reperfusion injury in perfused mouse liver pretreated with or without L-NAME. AU - Shibamoto,Toshishige, AU - Ruan,Zonghai, AU - Cui,Sen, AU - Liu,Wei, AU - Zhao,Zhan-Sheng, AU - Takano,Hiromichi, AU - Kurata,Yasutaka, AU - Koizumi,Tomonobu, AU - Kubo,Keishi, Y1 - 2007/02/09/ PY - 2006/04/05/received PY - 2006/06/06/revised PY - 2006/07/21/accepted PY - 2007/2/13/pubmed PY - 2007/5/18/medline PY - 2007/2/13/entrez SP - 30 EP - 5 JF - The Journal of surgical research JO - J Surg Res VL - 139 IS - 1 N2 - BACKGROUND: Hepatic ischemia-reperfusion (I/R) is accompanied by liver weight gain and ascites formation possibly caused by an increase in the sinusoidal pressure, a determinant of hepatic transvascular fluid movement. However, changes in the sinusoidal pressure during hepatic I/R in mice are not known. It is also controversial whether nitric oxide (NO) exerts a beneficial or detrimental effect on hepatic I/R injury. We determined the changes in hepatic sinusoidal pressure and liver weight, and the effect of a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) on I/R injury of isolated mouse liver. MATERIALS AND METHODS: Isolated liver from 20 male outbred ddY mice was perfused portally with diluted blood (Hct 3%). After pretreatment with L-NAME (100 microm) or D-NAME (100 microm), ischemia was induced at room temperature by occlusion of the inflow line of the portal vein for 1 h followed by 1-h reperfusion in a recirculating manner. The sinusoidal pressure was assessed by the double vascular occlusion pressure (Pdo), and pre- and postsinusoidal resistance was determined. Liver injury was assessed by blood levels of alanine aminotransferase (ALT). RESULTS: In the d-NAME group (n=7), immediately after reperfusion, the portal pressure increased by 2.8 +/- 0.1 (SE) mmHg, which was accompanied by an increase in Pdo of 1.5 +/- 0.1 mmHg, indicating increases in pre- and postsinusoidal resistance to a similar degree. Then, presinusoidal, but not postsinusoidal, resistance sustained increased until 60 min after reperfusion. Liver weight increased to 0.14 +/- 0.04 g/g liver after reperfusion, followed by a gradual return to baseline. Blood ALT levels increased at 60 min after reperfusion. There were no significant differences in changes in the variables between the D- and L-NAME (n=7) groups. In the time-matched non- I/R control group (n=6), no changes in variables were observed for 2 h. CONCLUSIONS: Mouse hepatic I/R causes marginal liver weight gain associated with a small and transient increase in the sinusoidal pressure, and nitric oxide does not play any significant roles in this injury. SN - 0022-4804 UR - https://www.unboundmedicine.com/medline/citation/17292416/The_sinusoidal_pressure_during_ischemia_reperfusion_injury_in_perfused_mouse_liver_pretreated_with_or_without_L_NAME_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-4804(06)00402-1 DB - PRIME DP - Unbound Medicine ER -