Medizinische Universität Graz - Research portal

Logo MUG Resarch Portal

Selected Publication:

Koeppel, TA; Thies, JC; Schemmer, P; Trauner, M; Gebhard, MM; Otto, G; Post, S.
Inhibition of nitric oxide synthesis in ischemia/reperfusion of the rat liver is followed by impairment of hepatic microvascular blood flow.
J Hepatol. 1997; 27(1):163-169 Doi: 10.1016/S0168-8278(97)80297-8
Web of Science PubMed FullText FullText_MUG Google Scholar

 

Co-authors Med Uni Graz
Schemmer Peter
Trauner Michael
Altmetrics:

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Abstract:
Recent studies provide evidence that nitric oxide (NO) has beneficial effects in hepatic ischemia/reperfusion injury. The purpose of this study was to evaluate whether nitric oxide is involved in the regulation of hepatic microvascular perfusion after warm hepatic ischemia. Therefore, we performed a study using in vivo fluorescence microscopy. Clamping of the left liver lobe was performed in male Wistar rats for the duration of 70 min. One experimental group (n=8) received L-NAME (Nw-nitro-L-arginine methyl ester hydrochloride), an NO-synthase inhibitor, 1 min prior to reperfusion. A second experimental group (n=8) received L-arginine (NO-substrate) continuously infused throughout the observation period. Controls (n=8) received equivalent volumes of an isotonic solution and underwent the same procedures. Hepatic microvascular blood flow and leukocyte-endothelial cell interaction was studied between 20 and 90 min after reperfusion using in vivo fluorescence microscopy. Inhibition of NO-synthesis during reperfusion by application of L-NAME caused a marked decrease in sinusoidal blood flow velocity. Furthermore, we noted an increase of non-perfused sinusoids in this group. Treatment with L-arginine improved functional perfusion of hepatic acini and reduced significantly the number of adherent leukocytes in sinusoids and venules compared to control animals. Our results provide further evidence that NO maintains postischemic hepatic microvascular perfusion and that inhibition of NO synthesis has detrimental effects on hepatic microhemodynamics during reperfusion.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Arginine - pharmacology
Blood Flow Velocity - drug effects
Cell Adhesion - drug effects
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiology
Enzyme Inhibitors - pharmacology
Leukocytes - drug effects
Leukocytes - physiology
Liver - blood supply
Liver - drug effects
Liver - physiopathology
Male -
Microcirculation - drug effects
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - antagonists & inhibitors
Rats -
Rats, Wistar -
Reperfusion Injury - physiopathology

Find related publications in this database (Keywords)
ischemia/reperfusion injury
liver
microcirculation
nitric oxide
© Med Uni GrazImprint