Blockade of NO with L-NAME jeopardize hepatic microcirculation during endotoxemia

The blockade of NO production during endotoxemia remains controversial. To evaluate the effect of NO blockade on the liver microcirculation, Sprague-Dawley male rats received LPS and 2h after they were treated by injections of L-NAME (10 mg/kg BW, n=6) or normal saline (NS, n=7). Intravital microscopy (IVM) assessed sinusoidal perfusion, blood samples were taken from the hepatic vein to determine base excess, and bile was collected. After 1h treatment L-NAME increased the LPS-induced sinusoidal perfusion failure (p < 0.05 vs NS), accentuated the acidosis in the hepatic blood effluent (p < 0.05 vs NS), while bile flow was further reduced (L-NAME 2.0 ± 0.5 vs NS 2.4 ± 0.1 <FONT FACE="Symbol">m</font>l/g/min). Non-selective NO blockade in endotoxemia enhances the sinusoidal perfusion failure, impairs acid-basic status of the liver and shows a tendency of impairment of the excretory function.

Nitric oxide; Hepatic microcirculation; Sinusoidal perfusion


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